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This chapter is under development. Some of it is collected from other chapters in Biochemistry Online. In this last chapter on binding, we will consider the daunting task faced by the immune system - to recognize all possible "foreign" molecules and react to them, either by targeting them for elimination, or, paradoxically, to recognize them but not react to them (a process called tolerance). The same can be said of "self-molecules". The immune system must recognize them but not respond to them, otherwise autoimmune disease might arise in which the body's powerful immune system targets self.
It is virtually impossible to give an in-depth description of the immune system in a short chapter. My goal is simply to illustrate how the immune system recognizes such a myriad of molecules and how, through signal transduction processes, it responds by becoming tolerant of the target, or promoting an immune response. To accomplish this impossible task, I will brief cover the innate and adaptive immune system and their differences, and how some cells (macrophages in particular) in the innate immune system and cells (B and T cells) in the adaptive immune response recognize and response to target molecules and cells. Emphasis will be given to recognition and sample signal transduction responses. Much of the info presented here comes from ideas presented in a fantastic book written by Lauren Sompayrac, How the Immune System Works. (2003, Blackwell Publishing. ISBN: 0-632-04702-X)
Three lines of defense protect us from the "enemies", foreign substances (bacteria, viruses and their associated proteins, carbohydrates, and lipids) collectively called antigens.
- physical barriers of cells that line our outside surface and our respiratory, GI tract, and reproductive system
- the innate immune system (IS) that all animals have. Composed of scavenger cells like macrophages (MΦ), neutrophils, dendritic cells, and natural killer cells (NK) that can move around the body through the blood and lymph systems and burrow into tissue to meet the enemy where they can engulf and destroy bacteria and "cellular debris". Macrophages start off as immature circulating monocytes which enter tissues by slipping through blood vessel walls, and in the process they differentiate into macrophages. There they lie in wait ready for the enemy.
- the adaptive immune system, which, as its name implies, can change and adapt to new molecular threats. This branch is better at dealing with viruses which do their damage inside of host cells.. The adaptive IS is comprised of B cells that make and secret protein antibodies that recognize specific foreign molecules, and T cells.
F1. Introduction to the Immune System - Biology
The Science of Biotechnology
Discovering and Developing Medicines
How Are Biotech Medicines Made?
The Science of Biotechnology
Biotechnology has been used in a rudimentary form since ancient brewers began using yeast cultures to make beer. The breakthrough that laid the groundwork for modern biotechnology came when the structure of DNA was discovered in the early 1950s. To understand how this insight eventually led to biotech therapies, it&rsquos helpful to have a basic understanding of DNA&rsquos central role in health and disease.
Illustration is copyrighted material of BioTech Primer, Inc., and is reproduced herein with its permission.
What does DNA do?
DNA is a very long and coiled molecule found in the nucleus, or command center, of a cell. It provides the full blueprint for the construction and operation of a life-form, be it a microbe, a bird, or a human. The information in DNA is stored as a code made up of four basic building blocks, called nucleotides. The order in which the nucleotides appear is akin to the order of the letters that spell words and form sentences and stories. In the case of DNA, the order of nucleotides forms different genes. Each gene contains the instructions for a specific protein.
With a few exceptions, every cell in an organism holds a complete copy of that organism&rsquos DNA. The genes in the DNA of a particular cell can be either active (turned on) or inactive (turned off) depending on the cell&rsquos function and needs. Once a gene is activated, the information it holds is used for making, or &ldquoexpressing,&rdquo the protein for which it codes. Many diseases result from genes that are improperly turned on or off.
Dendritic cells are a bit like spies sitting in among other cells. If they detect pathogens (foreign substances) within the body, they will ingest some, and molecules of the pathogens, called antigens, appear on the surface of the dendritic cell. The dendritic cell then leaves the site of infection and moves to the nearest lymph node. It stays there for about a week, displaying the antigens to the T and B cells that move through the lymph node.
Acknowledgement: Prof Gareth Jones, Wellcome Images
Macrophage means ‘big eater’. These cells ingest and clean up messes that include disabled cells or viruses that have been flagged with antibodies and dead cells.
Acknowledgement: MRC NIMR, Wellcome Images
2. Organism-Level Functions of the Immune System
The basic schema of vertebrate immunity consists of two evolutionary distinct ways to perceive the organism&rsquos external environment and to monitor its inner state. The first modality, more primitive and less refined in its perceptive mechanisms, is referred to as the &ldquoinnate&rdquo or &ldquonatural&rdquo immune system. This arm of immunity is composed of a variety of primordial phagocytes&mdash&ldquoeating cells&rdquo&mdashpossessing distinctive characteristics based on their tissue distribution. They ingest particulate microbes and destroy effete, cancerous, and damaged host cells. These immunocytes constitute the first line of the immune encounter and comprise the &ldquoresting&rdquo state of physiological immunity as they &ldquopolice&rdquo on-going processes of surveillance and restoration. This system has autonomous functions, but the incorporation of antigen (a substance that stimulates an immune response) may also lead to integration with the second mode of immunity, the so called, &ldquoacquired&rdquo immune system. This second arm of immunity has evolved mechanisms that are highly specific in their recognition capabilities and exhibit immune &ldquomemory&rdquo of previous sensitization. Acquired immunity is mediated by several classes of lymphocytes that may be stimulated by phagocyte first-encounters or as primary responders under certain pathological conditions. The B-lymphocytes produce antibody that recognizes antigens by structural homology and, correspondingly, T-cells have specific antigen-matching receptors on their cell surface. The initial recognition event leads to activation of a variety of effector reactions that destroy the immune target. However, the decision not to respond is also a recognition event and results in immune &ldquotolerance&rdquo. Both the innate and acquired immune cellular elements are regulated by a vast array of soluble molecular factors that serve to either activate or dampen immune responses. The complexity of diverse cell types, the mediators of their interactions, the contextual determinants that determine immune reactivity, and the wide range of physiological functions in which immunity participates, has defied comprehensive modeling. Consequently, immunology offers a fecund example of biological organizational complexity, which, in turn, leads to the fundamental philosophical question: On what basis is organismal identity established and maintained?
Immunology, from its earliest inception, has been concerned with biological identity&mdashits establishment and maintenance. In its original iteration, immunity was conceived as that function that preserved the integrity of the organism in terms of protecting and restoring its individuality. Thus, immune functions testified to the persistence of a stable, core identity defined in terms of its insularity and autonomy. Indeed, individuality undergirded the science from its inception, for the defense against pathogens was framed by an attacked patient (individual) pitted against alien others, the invaders. In this scenario, distinct borders mark individual identity, and immunity is the response to the violation of those boundaries. However, challenges to this conception of immunity have recently appeared. Emphasizing the contextual placement of the organism, notions of demarcated boundaries that have characterized traditional definitions of the organism are being revised.
Generally understood, an individual replicates itself and possesses anatomic borders, a harmonious communication between its parts, a division of labor for the benefit of the whole, and a system of hierarchical dominance and control. By these criteria, the immune system is responsible for establishing and maintaining the integrity of such an individual (Pradeu 2016). However, symbiosis challenges this entrenched definition of the individual organism: shared physiologies govern homeostasis anatomic margins lose clear definition development is intertwined among several phylogenetically defined entities and the unit of evolutionary selection becomes a multiplex genome (see the entry on the biological notion of individual). On this consortium view, notions of individuality are replaced with complexes of organisms that defy any singular definition of organismal identity as independent agents (Löwy 1991 S. Gilbert, Sapp, and Tauber 2012). In terms of commensal relationships, symbiosis, mediated by immune tolerance, signifies stabilized adaptation to the complex of diverse living elements that live in a cohesive ecology, both within and external to the traditional borders of the organism. When oriented by ecological relationships, immunology moves from its dominant concern with autonomous individuality to include the science of cooperative assemblies of organisms. The ontological implications of this re-formulation are highly significant for philosophical considerations of identity as discussed below (see the entry on identity).
2.1 Diachronic identity
The diachronic identity of an organism, its capacity to remain the same despite transformations, has puzzled philosophers since ancient Greece. Aristotle postulated the existence of immutable forms, that, being distinct from fluctuating matter, ensure the continued identity of living creatures (Categories, 3b22&ndash33 Metaphysics, Book D). Dissatisfied with this solution, Locke proposed that temporal identity of animals and plants is not ensured by their unvarying forms, but rather by the continuity of their lived life (Locke 1689, II.27.4 and II.27.8 Kaufman 2016). In the context of contemporary philosophy of biology, the importance of continuous identity was emphasized by Hull who argued that species lack essences and thus should be considered historical individuals with their own inner coherence and persistence conditions not unlike those of other living creatures (Hull 1978). He assumed that these persistence conditions are provided by continuity of changes in biological organization of these individuals so that only an abrupt disruption could cause a loss or change of identity (Hull 1992 Hull 1978: 355). This latter perspective has recently been adopted by advocates of animalism, who argue that continuity of physiological processes (organic animalism) or maintenance of characteristic structural organization (somatic animalism) are necessary for diachronic identity (Olson 1997 van Inwagen 1990 Mackie 1999 see the entry on animalism).
Immunology steps into the diachronic identity debate with Burnet&rsquos hypothesis that during embryonic development, the immune system learns to tolerate a defined set of molecules as &ldquoself&rdquo (Burnet 1959: 59). He proposed that autoreactive immune cells (lymphocytes) were purged during embryonic development to leave only those lymphocytes that ignore specific antigens encountered during this early stage (Burnet 1957). Defined negatively by a gap in the lymphocyte repertoire, immunological selfhood was assumed to persist in the adult as an invariant molecular &lsquoessence&rsquo of the organism, analogous to an unwavering psychological ego (Burnet 1959 Tauber 1994: 194). As observed by Pradeu and Carosella, this self/nonself model supported a substantialist view of identity in so far as it presupposed that the immune system ensures integrity of a preserved metaphysical core (Pradeu and Carosella 2006a: 246).
To provide a distinct view of the immune system&rsquos role in diachronic identity, Pradeu advocates the so-called &ldquogenidentity&rdquo view (Pradeu 2018). On this view, two objects are identical if their states are continuously connected over time (Lewin 1922). To specify which continuous states ensure temporal identity of an organism, Pradeu refers to those &ldquoimmune interactions [that] isolate some continuous biochemical interactions, which in turn individuate the organism&rdquo (Pradeu 2012: 248&ndash249). Accordingly, the immune system reacts to rapid molecular alterations in the pattern of biochemical interactions and thus helps to ensure that these interactions are continuous and unperturbed. Of note, which continuous process should be followed to define diachronic identity is not observer independent and must be adjusted to a particular theoretical perspective (Guay and Pradeu 2016: 318 Pradeu 2018).
However, the idea that the immune system contributes to organismal identity maintenance has to be weighed against evidence suggesting that immunity contributes to the accommodation of change. At the end of the nineteenth century, Metchnikoff proposed that phagocytes (primitive immune cells) were agents of organismal transformation, driving metamorphic and developmental alterations (Metchnikoff 1901  Tauber and Chernyak 1991). This early view has been supported by recent evidence that the immune system actively participates in mediating transformations in organismal identity by constantly redefining and modulating immune reactivity towards endogenous and exogenous molecules (Tauber 2017). This is most apparent during development as illustrated by the activity of brain-resident macrophages (microglia), which, by impacting angiogenesis/vascularization, as well as the migration, proliferation and apoptosis of neurons, influence social behavioral and sexual identity (Wynn, Chawla, and Pollard.2013 Lenz and Nelson 2018).
Tolerance of newly encountered antigens demonstrates the &ldquofluid&rdquo state of the reactive immune repertoire that undergoes alteration over the lifespan of the organism (Grignolio et al. 2014). And with a changing &ldquoimmune biography&rdquo, biological identity no longer conforms to the simple binary division of self and nonself that has hitherto characterized immune theorizing. Accordingly, animals have no immutable molecular essence that would ensure persistence of identity, at least as determined by immune tolerance or rejection (León-Letelier, Bonifaz, and Fuentes-Pananá 2019). Identity then becomes an ever-changing process of accepted transformations and rejected entries. From this vantage point, the animalist definitions of diachronic identity as a mere persistence of life or even an underlying constancy fails to account for the dynamic quality of immune-mediated identity transitions (van Inwagen 1990: 148&ndash149 Olson 1997 Mackie 1999 Roy and Hebrok 2015 Dupré 2017). Consequently, the immune processual point of view defines organismal persistence as &ldquoa coordinated group of changes&rdquo rather than as an invariant state or a continuous connection between such states. This understanding has important implications for philosophy of biology and ontology, more generally (Dupré 2014 Nicholson and Dupre 2018 Meincke 2018).
2.2 Synchronic identity
While diachronic identity of an organism is understood as its persistence though time, synchronic identity is defined in terms of its individuality or distinctiveness (Sober 2000: 154). Attempts have been made to identify distinguishing characteristics such as functional autonomy, possession of mutually interdependent parts, genetic homogeneity and spatial boundaries (Clarke 2010). Others, pointing to the heterogeneous character of biological individuals, have argued that no sole feature can serve as a universal determinant of individuality (see the entry on the biological notion of individual). Part of the contention resides in differing frames of reference of study: Most considerations of synchronic individuality focus upon evolutionary individuals as units of selection (Gould and Lloyd 1999) that differs from how physiological individuals might be distinguished (Pradeu 2016). Regardless of their involvement in evolution, organisms exhibit various levels of physiological and morphological integration that makes their indivisibility problematic (Godfrey-Smith 2009). Immunology contributes to discussions of individuality in this latter sense by considering the role of the immune system in defining the boundaries of the organism by the functional measures of rejection or assimilation.
Pradeu formulated such criteria and proposed that the immune system plays the central role in determining what is included in the organism and what is not (Pradeu 2012). The differentiation is based on his continuity/discontinuity model, which depicts the immune system reacting to transient alterations in the pattern of antigen receptor interactions and tolerates long-lasting modifications (Pradeu, Jaeger, & Vivier 2013 Pradeu & Carosella 2006a: 241, 2006b). Such a mechanism is based on recognizing that autoimmunity is a normal function of immunity (Tauber 2015). Because host antigens do not evoke an immune response, a stable, &ldquocontinuity&rdquo of immune interactions establishes an activation threshold that initiates an immune response only upon a rapid increase in antigenic load. The immune system thus distinguishes the stable state of tolerant recognition of tonic signals arising from normal physiological process in contrast to the appearance of novel antigens, for example, arising from pathogen invasion or tissue injury (Grossman and Paul 1992 Myers, Zikherman and Roose 2017 Pradeu 2012: 246 Grossman 2019). Thus the development of tolerance to frequently encountered antigens, commensals, tissue grafts and anastomosed animals results in the establishment of stable, integrated associations mediated by low-grade immune interactions (Pradeu and Carosella 2006a, 2006b Pradeu 2012: 251&ndash252). In this formulation, the immune system plays a central role in defining an individual by permitting beneficial physiological inclusion of heterologous components.
Others refer to these stable immune interactions with microbiota to deny that organisms are individuals (S. Gilbert, Sapp, and Tauber 2012). Appreciating the ubiquity of symbiosis, the immune system from this point of view becomes a key mediator of the holobiont by tolerating and coordinating microbial-host relationships. On this basis, these critics highlight that most of these interactions fall on a dynamic spectrum of rejection and acceptance making it impossible, in principle, to determine the boundaries of individuality. Symbiotic interactions do not conform to a simple acceptance-rejection model. Rather, to attune its responses to microbial signals the immune system launches a broad spectrum of T-cell reactions in combination with a variety of innate immune and tissue cell-derived signals (cytokines, hormones, neurotransmitters) in combination with complex regulatory controls (Eberl 2016). As suggested by Cohen, immunity is the product of an active computational state that constantly assesses the state of the organism&rsquos internal state and the surroundings in which it lives (Cohen 2007a, 2007b). In the context of such fluid activity, transitioning from one unique activation state to another does not allow definitive delineation of organismal borders. Instead, the immune system acts as gatekeeper that controls the apparent boundary between the organism and its environment (Tauber 2008: 231 Tauber 2017 S. Gilbert, Sapp, and Tauber 2012). From this perspective, the view of immunity as protecting insularity shifts to recognizing its role in establishing and maintaining communal relationships that blur the distinction of an atomistic insular individuality (Skillings 2016).
The self/nonself, tolerance/response dichotomies collapse altogether, when considered in the context of mammalian pregnancy, where various modalities are employed to preserve the temporary immune sanctuary of the &lsquoforeign&rsquo fetus (Howes 2007 A. Martin 2010). Studies of immune-mediated exchanges between the mother and the fetus not only challenge our view of immunity as concerned with rejection and defense, but also transform our understanding of biological individuality (Erlebacher 2013 Howes 2008). More specifically, recent studies undermine the vision of the maternal immune system as antagonistic to the fetus and rather point to active immune participation in the formation of an amalgamated maternal-fetal individual, whose ontological status lies at the continuum between unification and distinctiveness (Howes 2008). Delineation of the role of inflammation during blastocyst implantation further supports this interactive vision, demonstrating that instead of acting as a rejection response, inflammation promotes a mutually tolerant fusion between the embryo and the mother (Griffith et al. 2017 Mor, Aldo, and Alvero 2017). Indeed, the transformation of an inflammation-induced reaction pathway into a cell differentiation pathway in decidual stromal cells exhibits the intimate connection of the immune and reproductive systems in eutherians (G. Wagner, Erkenbrack, and Love 2019 Nuño de la Rosa, Pavlicev, and Etxeberria 2019, in Other Internet Resources).
In conclusion, despite significant contributions of philosophy of immunology to debates about identity, no straightforward answer to the question of how the immune system contributes to biological individuality has been offered. Considering the actual individualization practices in various fields of biology, it may well be concluded that no single account of the biological individual suffices and that the question of whether particular criteria are valid or not depends on the research perspective adopted. Part of the conundrum may lie in the efforts to consider the issue at the metaphysical, rather than at the epistemological level (Love 2018, Love and Brigandt 2017). As discussed below, the status of the &ldquoimmune self&rdquo is a fecund case in point.
2.3 The immune self
Wide use of the self/nonself distinction in different clinical and research traditions (provided by the relaxed and varied meanings associated with its use) has established such discrimination as the governing construct of the science (e.g., Howes 2010 Hoffman 2012 Cohn 2015). Indeed, the &ldquoimmune self&rdquo has served as immunology&rsquos foundational concept to order immune theorizing for the past 70 years (Burnet and Fenner 1949 Tauber 1994). However, despite the paradigm&rsquos established standing, definition of immune identity has proven elusive. As discussed above (section 2.1), because of fluctuations of immune activity over the lifespan of the organism, conceptualizing and modeling active tolerance have yet to yield criteria for defining stable identity (Bilate and LaFaille 2012). Moreover, a consensus definition of selfhood has remained elusive inasmuch as different investigative frameworks promote differing characteristics of immune identity based on their respective structural and functional criteria (Matzinger 1994). Critics have therefore questioned the immune self&rsquos standing and utility (e.g., Matzinger 1994 Tauber 2000 Pradeu 2012). The latter position argues that the &ldquoself&rdquo might be better regarded as only a metaphor for a &ldquofigure&rdquo outlined by the immune system&rsquos silence, i.e., its non-reactivity. Such a functionally flexible definition has been resisted. Defenders argue that the notion of stabilized discrimination correctly depicts the immune system&rsquos organizing functions (which converge on defending a well-demarcated organism), and that efforts to eliminate or modify this metaphor are misguided attempts to &ldquopolice&rdquo borders between science and culture (Anderson 2014 Hoffman 2012). Drawing from the philosophical canon, Howes referred to Hume to argue that realism about self (immune or otherwise) can be saved despite the dependency of context and the ever-changing character of the postulated ego (Howes 1998). She suggested that the efforts to deny the reality of the self are based on its non-substantial character and thus reflects entrenched substantialist assumptions. She proposed that a middle ground exists between substantial self and no-self by adopting a processual, understanding of selfhood (Howes 1999).
While the standing of the immune self has remained contentious, epistemological ambiguity and flexible polysemy has proven effective in sustaining the term&rsquos powerful heuristic value as an idiom with many uses and meanings (Crist and Tauber 2000). Its versatility and pragmatic utility have effectively integrated clinical immune phenomena by highlighting the essential similarity or interconnectedness of diverse immune-mediated processes in response to various clinical challenges. Thus nutrition, allergy, infection, autoimmune disease, various phenomena of tolerance, natural or experimentally created chimeras (transplantation), and autoimmunity all become conceived as a network of interlinked or interrelated functions subject to evolutionary transformation and adaption. As these topics mirror and play off one another under the rubric of selfhood, immunologists have a ready means by which to represent states or processes that arise in the various interactions between the organism and its environment at different evolutionary stages and development.
Finally, the self&rsquos appearance in immunology served as a readily understood shorthand reference to personal identity, and the efforts to substantiate that extrapolation on its own terms guided the discipline for the latter half of the twentieth century (for historical case studies see Löwy 1991). After all, beyond the experimental science, the interpretative context of immune selfhood draws from wider social meanings of individuality and insularity (Tauber 2016 see below, section 5.0). The autonomous construction of identity resonates with Western civic ideals and in turn supports them by melding laboratory findings with various extrapolated or borrowed philosophical, political and psychological formulations of human agency. And conversely, immunology has been studied as a source of important metaphors and other tropes feeding back on the science&rsquos supporting culture to transform understanding of agency and communal relationships (discussed below, section 5.0).
3. Two men who unraveled the immune system's functions were bitter rivals.
Two scientists who discovered key functions of the immune system, Louis Pasteur and Robert Koch, should have been able to see their work as complementary, but they wound up rivals. Pasteur, a French microbiologist, was famous for his experiments demonstrating the mechanism of vaccines using weakened versions of the microbes. Koch, a German physician, established four essential conditions under which pathogenic bacteria can infect hosts, and used them to identify the Mycobacterium tuberculosis bacterium that causes tuberculosis. Though both helped establish the germ theory of disease—one of the foundations of modern medicine today—Pasteur and Koch's feud may have been aggravated by nationalism, a language barrier, criticisms of each other's work, and possibly a hint of jealousy.
How does the immune system combat coronavirus? Case study brings a vaccine closer
These preliminary findings lay the groundwork for an effective vaccine and treatment for COVID-19.
Two of the biggest questions scientists have about the new coronavirus COVID-19 are how to fight it with medication, and how to support the body's own defenses against the virus.
In a case study published Monday, March 16 as a letter in the journal Nature Medicine, researchers finally offer some clues to at least the second question.
By sequencing the immune response of a person with confirmed, mild-to-moderate COVID-19, researchers pinpointed exactly which of the body's own immune cells attack the new coronavirus. If these preliminary results bear out in others with the virus, they could lead to an effective treatment and vaccine.
"This is an incredible step forward in understanding what drives recovery of COVID-19,” Katherine Kedzierska, a co-author on the new study and researcher at the Peter Doherty Institute for Infection and Immunity, said in a statement.
“People can use our methods to understand the immune responses in larger COVID-19 cohorts, and also understand what's lacking in those who have fatal outcomes."
The case study focuses on one person, so the findings cannot be applied to everyone with the infection. But they do offer tantalizing hints as to what happens when the body starts to defend itself against COVID-19.
“We have to be careful because the study of one person is very difficult to generalize to a broad population,” Mark Slifka, a microbiologist at Oregon Health and Science University who was not involved in the case study, tells Inverse.
At this stage, these clues to the body's immune response provides a jumping off point for researchers to better predict who might recover from COVID-19, and how fast they'll get better.
Window into recovery
In the new case study, scientists tracked the immune response of a 47-year-old woman who successfully fought off a mild-to-moderate COVID-19 infection. The woman was one of the first coronavirus cases confirmed in Australia. It is thought that she came down with COVID-19 after traveling from Wuhan, China, to Melbourne, Australia.
The otherwise healthy woman's COVID-19 symptoms included lethargy, a sore throat, dry cough, chest pains, trouble breathing, and a fever. She presented to a Melbourne hospital and recovered within two weeks of presentation.
Throughout the woman's illness, researchers observed her symptoms and took blood samples at four different time points during her hospitalization. They then sequenced which immune cells were present in her blood, charting both when they appeared and disappeared.
Their results suggest the immune system launches a similar attack on the new coronavirus as it does on the seasonal flu.
Three days before the woman's symptoms faded, the researchers looked at levels of four types of immune cells that activated to fight COVID-19: antibody-secreting cells, follicular helper T cells, activated CD4+ T cells and CD8+ T cells and immunoglobulin M, and IgG antibodies that bound the COVID-19-causing coronavirus.
"We showed that even though COVID-19 is caused by a new virus, in an otherwise healthy person, a robust immune response across different cell types was associated with clinical recovery, similar to what we see in influenza," Kedzierska said.
“Her immune responses did a great job,” Kedzierska told Bloomberg at the time the case study was published.
Tracking these immune cells, which are often a “tell-tale” sign of recovery during seasonal flu infection, enabled the researchers to predict the patient’s recovery, Oanh Nguyen, a case study co-author and researcher at the Doherty Institute, said in the same statement accompanying the research.
How does COVID-19 compare to other infections?
This immune response resembles how the body responds to other infections, Slifka says.
"We know that people are able to clear this infection and they are mounting strong immune responses — both T cell responses and eventually antibody responses," he says.
"This is how we deal with infection whether it is the flu or the seasonal cold virus or COVID-19."
The researchers on the new study hope to replicate their analysis in other people with COVID-19. Ultimately, they want to understand why certain demographics have trouble fighting COVID-19, while others seem to be protected.
"We hope to now expand our work nationally and internationally to understand why some people die from COVID-19, and build further knowledge to assist in the rapid response of COVID-19 and future emerging viruses," Irani Thevarajan, a co-author on the new case study and researcher at the Doherty Institute, said in a statement.
An Immune System for our Microbial World
In this video, you will see a high-level overview of the immune system at work in the context of daily life. What is seen here equally applies to transmission and the body’s reaction to a coronavirus. The immune system mounts a response against pathogens as they infect an individual and replicate. The response includes both an immediate innate response and a slower adaptive response, which are explained in greater detail in the following sequence. This video features HMX Fundamentals Immunology faculty member Andrew Lichtman of Harvard Medical School.
Introduction to the Innate Immune Response
The innate immune response forms the first line of defense against invading pathogens. Innate immunity includes barriers and a variety of cells and molecules that are part of the rapid response to threats to our health. In this interactive you will be introduced to the various aspects of the innate immune response and the ways in which they work together to prevent and control infection. While the immune system protects us from many pathogens, the inflammation that occurs as part of the immune response can also damage our own tissues and impair the function of our organs when pathogens stimulate a very strong response.
Top reviews from the United States
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I bought this textbook because it was required for my undergraduate-level immunology class, but it would also be great for anyone who is learning immunology on their own. The way it is written makes it very easy to understand, and there are many colorful drawings that help explain what you are reading. It doesn't drag as much as other textbooks seem to. I actually find myself reading ahead of class because it's just so painless to read. There are a few things I might change about it, but compared to the many other horrible textbooks I've been subjected to, these imperfections are almost unnoticeable (a typo here and there, etc.). Some people in class are complaining that some of the drawings could be less confusing if they were colored differently, but I have not found that to be a problem at all. If you read the captions underneath the drawings like you're meant to, it makes perfect sense. I have the softcover version, and it's perfect for people who like to write tons of notes in the margins as they learn. This is a textbook that I will definitely be keeping for further reference, so I write all over it and use it as my notebook for class. There are areas I wish would go into further detail, but I can understand why an introductory textbook would leave those details out, as a class is only so many weeks long. The book is detailed enough that you should be able to access *and actually understand* most journal articles online regarding whatever aspect of immunology you wish to know more about. I've had good luck with books published by Garland Science in the past (Introduction to Protein Structure is a good one).
You should be able to understand the book without taking microbiology, but a knowledge of micro will make it more interesting. A shaky background in molecular biology/genetics is good enough, but again, it will be more interesting if you brush up on this beforehand. The textbook mentions a great deal of problems in immunology that have yet to be solved, and if you have a background in these other areas, it makes it more intriguing to ponder possible solutions and to think about the impact these solutions would have on the scientific community and on society.
Immunology is not usually regarded as one of those subjects that lends itself to easy understanding. I feel this book does a better than average job of describing how this confusing part of human physiology works. Everything is described in enough detail for an undergraduate senior level class, assuming one has a decent grasp of how biochemistry and/or molecular biology works. It makes it easier to make this subject easier to understand or maybe even enjoyable.
I purchased the Kindle textbooks version which works with the non-Windows 8 app store (AKA:Metro) version of the Kindle app. The Windows 8 app doesn't support Kindle textbooks for some reason. That said this Kindle version works great with iPad 2 and the Kindle app for Windows Vista and 7. It is really nice to be able to do screen grabs of illustrations for reviewing material with the Onenote screen clipping tool.
Studied from this book in college back in 2011. The first 4ish chapters lay the groundworks for the entire book. I was able to hardcore study those chapters and then breeze the rest of the way though the book and class. Things from here have stuck with me now in 2015.
It might be basic for someone already in the field. For premeds or bio and/or Chemistry majors this gives a perfect amount of working knowledge to succeed in your career field.
Diagram of the Human Immune System (Infographic)
The immune system protects the body against disease or other potentially damaging foreign bodies. When functioning properly, the immune system identifies and attacks a variety of threats, including viruses, bacteria and parasites, while distinguishing them from the body’s own healthy tissue.
The Lymphatic system consists of bone marrow, spleen, thymus and lymph nodes.
Bone marrow produces white blood cells, or leukocytes.
The spleen is the largest lymphatic organ in the body contains white blood cells that fight infection or disease.
The thymus is where T-cells mature. T-cells help destroy infected or cancerous cells.
Lymph nodes produce and store cells that fight infection and disease.
Lymphocytes and leukocytes are small white blood cells that play a large role in defending the body against disease.
The two types of lymphocytes are B-cells, which make antibodies that attack bacteria and toxins, and T-cells, which help destroy infected or cancerous cells.
As a biology major, you will engage in scientific investigation of nature, from the molecular level to entire ecosystems, developing skills to address the challenges related to the natural world.
In addition to classroom instruction, our curriculum emphasizes firsthand observation and experimentation in both the laboratory and the field. You’ll have the opportunity to work closely with faculty mentors who are active scholars, publishing research that spans a broad range of biological subdisciplines, including marine, cell and molecular biology. You’ll learn how to critically assess a scientific problem, collect and analyze data, and write and speak about biology for general and technical audiences while taking advantage of Oxy’s unique location at the nexus of three distinctive ecosystems—the Pacific Ocean, the San Gabriel Mountains, and the Mojave Desert.
International opportunities for field research also are plentiful, including study at La Selva Biological Station in Costa Rica, where students have the chance to conduct research alongside professors and scientists each summer. Our forthcoming Genomics Center in the Anderson Center for Environmental Science will unite new DNA sequencing technologies with museum specimens from our world-renowned biodiversity collections, including the largest collection of Mexican birds in the world housed in the Moore Lab of Zoology and the stunning 117,000-piece Cosman Shell Collection. Our Vantuna Research Group features both the longest continual time series studies of rocky reefs in the world and the largest spatial scale studies of reefs in the Southern California Bight.
After studying the evolutionary unity, diversity, and complexity of biological systems, you will be prepared for a variety of postgraduate options, including medicine, public health, ecology, environmental science, education, health communication, and graduate work in the sciences. Biology also opens the door to many other possibilities not traditionally associated with the sciences, such as government, business, policy and industry work.