13: Humoral Immunity - Biology

13: Humoral Immunity - Biology

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Humoral Immunity refers to the production of antibody molecules in response to an antigen. These antibody molecules circulate in the plasma of the blood and enter tissue and organs via the inflammatory response. Humoral immunity is most effective microbes or their toxins located in the extracellular spaces of the body. Antibodies or immunoglobulins are specific glycoprotein configurations produced by B-lymphocytes and plasma cells in response to a specific antigen and capable of reacting with that antigen.

How Immunity Generated from COVID-19 Vaccines Differs from an Infection

A key issue as we move closer to ending the pandemic is determining more precisely how long people exposed to SARS-CoV-2, the COVID-19 virus, will make neutralizing antibodies against this dangerous coronavirus. Finding the answer is also potentially complicated with new SARS-CoV-2 “variants of concern” appearing around the world that could find ways to evade acquired immunity, increasing the chances of new outbreaks.

Now, a new NIH-supported study shows that the answer to this question will vary based on how an individual’s antibodies against SARS-CoV-2 were generated: over the course of a naturally acquired infection or from a COVID-19 vaccine. The new evidence shows that protective antibodies generated in response to an mRNA vaccine will target a broader range of SARS-CoV-2 variants carrying “single letter” changes in a key portion of their spike protein compared to antibodies acquired from an infection.

These results add to evidence that people with acquired immunity may have differing levels of protection to emerging SARS-CoV-2 variants. More importantly, the data provide further documentation that those who’ve had and recovered from a COVID-19 infection still stand to benefit from getting vaccinated.

These latest findings come from Jesse Bloom, Allison Greaney, and their team at Fred Hutchinson Cancer Research Center, Seattle. In an earlier study, this same team focused on the receptor binding domain (RBD), a key region of the spike protein that studs SARS-CoV-2’s outer surface. This RBD is especially important because the virus uses this part of its spike protein to anchor to another protein called ACE2 on human cells before infecting them. That makes RBD a prime target for both naturally acquired antibodies and those generated by vaccines. Using a method called deep mutational scanning, the Seattle group’s previous study mapped out all possible mutations in the RBD that would change the ability of the virus to bind ACE2 and/or for RBD-directed antibodies to strike their targets.

In their new study, published in the journal Science Translational Medicine, Bloom, Greaney, and colleagues looked again to the thousands of possible RBD variants to understand how antibodies might be expected to hit their targets there [1]. This time, they wanted to explore any differences between RBD-directed antibodies based on how they were acquired.

Again, they turned to deep mutational scanning. First, they created libraries of all 3,800 possible RBD single amino acid mutants and exposed the libraries to samples taken from vaccinated individuals and unvaccinated individuals who’d been previously infected. All vaccinated individuals had received two doses of the Moderna mRNA vaccine. This vaccine works by prompting a person’s cells to produce the spike protein, thereby launching an immune response and the production of antibodies.

By closely examining the results, the researchers uncovered important differences between acquired immunity in people who’d been vaccinated and unvaccinated people who’d been previously infected with SARS-CoV-2. Specifically, antibodies elicited by the mRNA vaccine were more focused to the RBD compared to antibodies elicited by an infection, which more often targeted other portions of the spike protein. Importantly, the vaccine-elicited antibodies targeted a broader range of places on the RBD than those elicited by natural infection.

These findings suggest that natural immunity and vaccine-generated immunity to SARS-CoV-2 will differ in how they recognize new viral variants. What’s more, antibodies acquired with the help of a vaccine may be more likely to target new SARS-CoV-2 variants potently, even when the variants carry new mutations in the RBD.

It’s not entirely clear why these differences in vaccine- and infection-elicited antibody responses exist. In both cases, RBD-directed antibodies are acquired from the immune system’s recognition and response to viral spike proteins. The Seattle team suggests these differences may arise because the vaccine presents the viral protein in slightly different conformations.

Also, it’s possible that mRNA delivery may change the way antigens are presented to the immune system, leading to differences in the antibodies that get produced. A third difference is that natural infection only exposes the body to the virus in the respiratory tract (unless the illness is very severe), while the vaccine is delivered to muscle, where the immune system may have an even better chance of seeing it and responding vigorously.

Whatever the underlying reasons turn out to be, it’s important to consider that humans are routinely infected and re-infected with other common coronaviruses, which are responsible for the common cold. It’s not at all unusual to catch a cold from seasonal coronaviruses year after year. That’s at least in part because those viruses tend to evolve to escape acquired immunity, much as SARS-CoV-2 is now in the process of doing.

The good news so far is that, unlike the situation for the common cold, we have now developed multiple COVID-19 vaccines. The evidence continues to suggest that acquired immunity from vaccines still offers substantial protection against the new variants now circulating around the globe.

The hope is that acquired immunity from the vaccines will indeed produce long-lasting protection against SARS-CoV-2 and bring an end to the pandemic. These new findings point encouragingly in that direction. They also serve as an important reminder to roll up your sleeve for the vaccine if you haven’t already done so, whether or not you’ve had COVID-19. Our best hope of winning this contest with the virus is to get as many people immunized now as possible. That will save lives, and reduce the likelihood of even more variants appearing that might evade protection from the current vaccines.

Bloom Lab (Fred Hutchinson Cancer Research Center, Seattle)

NIH Support: National Institute of Allergy and Infectious Diseases

Evolution of antibody immunity to SARS-CoV-2

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has infected 78 million individuals and is responsible for over 1.7 million deaths to date. Infection is associated with the development of variable levels of antibodies with neutralizing activity, which can protect against infection in animal models 1,2 . Antibody levels decrease with time, but, to our knowledge, the nature and quality of the memory B cells that would be required to produce antibodies upon reinfection has not been examined. Here we report on the humoral memory response in a cohort of 87 individuals assessed at 1.3 and 6.2 months after infection with SARS-CoV-2. We find that titres of IgM and IgG antibodies against the receptor-binding domain (RBD) of the spike protein of SARS-CoV-2 decrease significantly over this time period, with IgA being less affected. Concurrently, neutralizing activity in plasma decreases by fivefold in pseudotype virus assays. By contrast, the number of RBD-specific memory B cells remains unchanged at 6.2 months after infection. Memory B cells display clonal turnover after 6.2 months, and the antibodies that they express have greater somatic hypermutation, resistance to RBD mutations and increased potency, indicative of continued evolution of the humoral response. Immunofluorescence and PCR analyses of intestinal biopsies obtained from asymptomatic individuals at 4 months after the onset of coronavirus disease 2019 (COVID-19) revealed the persistence of SARS-CoV-2 nucleic acids and immunoreactivity in the small bowel of 7 out of 14 individuals. We conclude that the memory B cell response to SARS-CoV-2 evolves between 1.3 and 6.2 months after infection in a manner that is consistent with antigen persistence.

Conflict of interest statement

Competing interests The Rockefeller University has filed a provisional patent application in connection with this work on which D.F.R. and M.C.N. are inventors (US patent 63/021,387). R.E.S. is on the scientific advisory board of Miromatrix Inc and is a consultant and speaker for Alnylam Inc. S.M. has served as a consultant for Takeda Pharmaceuticals, Morphic and Glaxo Smith Kline. Z.Z. received seed instruments and sponsored travel from ET Healthcare.


Extended Data Fig. 1 |. Clinical correlates…

Extended Data Fig. 1 |. Clinical correlates of plasma antibody titres.

Extended Data Fig. 2 |. Correlations of…

Extended Data Fig. 2 |. Correlations of plasma antibody measurements.

Extended Data Fig. 3 |. Persistent longitudinal…

Extended Data Fig. 3 |. Persistent longitudinal changes in the phenotypic landscape of B cells…

Extended Data Fig. 4 |. Flow cytometry.

Extended Data Fig. 4 |. Flow cytometry.

Extended Data Fig. 5 |. Frequency distributions…

Extended Data Fig. 5 |. Frequency distributions of human V genes.

Extended Data Fig. 6 |. Analysis of…

Extended Data Fig. 6 |. Analysis of antibody somatic hypermutation of persisting clones, CDR3 length…

Extended Data Fig. 7 |. ELISA of…

Extended Data Fig. 7 |. ELISA of wild-type or mutant RBD for monoclonal antibodies.

Extended Data Fig. 8 |. Neutralization of…

Extended Data Fig. 8 |. Neutralization of wild-type and mutant RBDs, C51 alignment and binding…

Extended Data Fig. 9 |. SARS-CoV-2 antigen…

Extended Data Fig. 9 |. SARS-CoV-2 antigen in human enterocytes in the gastrointestinal tract at…

Extended Data Fig. 10 |. SARS-CoV-2 antigen…

Extended Data Fig. 10 |. SARS-CoV-2 antigen and RNA is detectable in different intestinal segments…

Fig. 1 |. Plasma antibody dynamics against…

Fig. 1 |. Plasma antibody dynamics against SARS-CoV-2.

Fig. 2 |. Sequences of anti-SARS-CoV-2 RBD…

Fig. 2 |. Sequences of anti-SARS-CoV-2 RBD antibodies.

Fig. 3 |. Reactivity of anti-SARS-CoV-2 RBD…

Fig. 3 |. Reactivity of anti-SARS-CoV-2 RBD monoclonal antibodies.

Fig. 4 |. Neutralizing activity of anti-SARS-CoV-2…

Fig. 4 |. Neutralizing activity of anti-SARS-CoV-2 RBD monoclonal antibodies.

Immunobiology: The Immune System in Health and Disease. 5th edition.

Many of the bacteria that cause infectious disease in humans multiply in the extracellular spaces of the body, and most intracellular pathogens spread by moving from cell to cell through the extracellular fluids. The extracellular spaces are protected by the humoral immune response, in which antibodies produced by B cells cause the destruction of extracellular microorganisms and prevent the spread of intracellular infections. The activation of B cells and their differentiation into antibody-secreting plasma cells (Fig. 9.1) is triggered by antigen and usually requires helper T cells. The term ‘helper T cell’ is often used to mean a cell from the TH2 class of CD4 T cells (see Chapter 8), but a subset of TH1 cells can also help in B-cell activation. In this chapter we will therefore use the term helper T cell to mean any armed effector CD4 T cell that can activate a B cell. Helper T cells also control isotype switching and have a role in initiating somatic hypermutation of antibody variable V-region genes, molecular processes that were described in Chapter 4.

Figure 9.1

The humoral immune response is mediated by antibody molecules that are secreted by plasma cells. Antigen that binds to the B-cell antigen receptor signals B cells and is, at the same time, internalized and processed into peptides that activate armed helper (more. )

Antibodies contribute to immunity in three main ways (see Fig. 9.1). To enter cells, viruses and intracellular bacteria bind to specific molecules on the target cell surface. Antibodies that bind to the pathogen can prevent this and are said to neutralize the pathogen. Neutralization by antibodies is also important in preventing bacterial toxins from entering cells. Antibodies protect against bacteria that multiply outside cells mainly by facilitating uptake of the pathogen by phagocytic cells that are specialized to destroy ingested bacteria. Antibodies do this in either of two ways. In the first, bound antibodies coating the pathogen are recognized by Fc receptors on phagocytic cells that bind to the antibody constant C region (see Section 4-18). Coating the surface of a pathogen to enhance phagocytosis is called opsonization. Alternatively, antibodies binding to the surface of a pathogen can activate the proteins of the complement system, which was described in Chapter 2. Complement activation results in complement proteins being bound to the pathogen surface, and these opsonize the pathogen by binding complement receptors on phagocytes. Other complement components recruit phagocytic cells to the site of infection, and the terminal components of complement can lyse certain microorganisms directly by forming pores in their membranes. Which effector mechanisms are engaged in a particular response is determined by the isotype or class of the antibodies produced.

In the first part of this chapter we will describe the interactions of B cells with helper T cells that lead to the production of antibodies, the affinity maturation of this antibody response, the isotype switching that confers functional diversity, and the generation of memory B cells that provide long-lasting immunity to reinfection. In the rest of the chapter we will discuss in detail the mechanisms whereby antibodies contain and eliminate infections.

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NEW (2016) AQA AS-Level Biology – Humoral Immunity & Antibodies

I am a secondary school & A-level Science teacher, specialising in Biology. I am also an experienced AQA GCSE Biology Examiner. My resources contain a mix of Biology, Chemistry and Physics lessons aimed at meeting specification points for the new AQA Trilogy GCSE course and KS3 Activate course. All of my lessons include at least one opportunity for self-assessment, a range of activities to suit students of all abilities, a set of differentiated starter questions and a plenary.

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This lesson is designed for the NEW AQA AS-level Biology course, particularly the ‘Cells’ module.

For more lessons designed to meet specification points for the NEW AQA A-level Biology course please visit my shop:

A-Level lesson format: I teach in more of a lecture style compared to GCSE. In the majority of my A-level lessons the beginning portion of the lesson is mainly teacher-led, where students are expected to take notes onto a handout/in their books. This is then mixed in with student-led activities, as well as questions and exam prep.

You will find some of my slides have blank spaces for you to add more detail/descriptions/explanations. If you look at the ‘Notes’ section underneath each of these slides, you will find additional content which you can add in as you teach!

This lesson on humoral immunity & antibodies begins with a starter discussion to get students to describe the role of cytotoxic t-cells, and the role of lysosomes during phagocytosis. They should also discuss the fate of cloned t-cells during a cell-mediated immune response.

Humoral immunity is defined first, and students are asked to consider why the term humoral is used. Then, students will fill in gaps on their worksheet as humoral immunity is further explained. There are extra notes below the slide, and the answers will appear for self-assessment.

The next slide sets out a diagram of humoral immunity, then students are asked to arrange the process by sequencing sentences, then self-assess.

In pairs, students will then be given information on either plasma cells or memory cells and teach each other about the cell they’ve been assigned. Each student should complete descriptions of both types in their books.

Students are then asked to consider why lymphocytes don not attack their own cells and taught the significance of lymphocytes development in the foetus.

The next task is to sort information cards into categories cell-mediated, humoral, or both. They can self-assess this task to the following slide.

Students are then introduced to the structure of antibodies. They will watch a video, and answer seven questions, including a diagram. They can self-assess to the slide before considering how antibodies lead to the destruction pathogens. Students are also asked to consider why it is important that antibodies have two antigen binding sites.

The plenary is to spend a full minute discussing with a partner what they have learned from this lesson.

All resources are included. Thanks for looking, if you have any questions please let me know in the comments section and any feedback would be appreciated :)


All participants gave informed written consent in accordance with ethical approval from the local ethics committee [Oxford Research Ethics Committee (OxREC) C approval number 12/SC/0407. EudraCT number 2012-002443-26]. Ninety 14- to 26-mo-old healthy children received two doses of TIV or ATIV at 4-wk intervals during the 2012� winter season. Antibody titers were measured by HAI and the data were log-transformed to calculate the GMT and GMR (ratio) with 95% confidence intervals (CI). Plasmablast and memory B-cell responses were quantitated by ELISpot. T-cell cytokine profiles were characterized by flow cytometry. Total RNA was extracted from blood and checked for quality before amplification, labeling, hybridization, and scanning (Affymetrix). Expression differences were calculated for each subject/time point, and difference of mean difference was assessed by one-sample Student t test. GSEA was performed using BTMs as gene sets. Probe sets were ranked based on fold-change relative to preimmunization or based on correlation between expression fold-change relative to preimmunization and HAI response. GSEA was run in preranked list mode with 1,000 permutations to generate normalized enrichment scores for the BTMs based on the distribution of member genes of each module in the ranked list.

See SI Methods for details and additional references (23 �).


Much remains to be learned regarding coronavirus immunity in general and SARS-CoV-2 immunity in particular, including the protective immunity induced by vaccines and the maintenance of immunity against this virus. Furthermore, multiple vaccine types will probably be needed across different populations (eg, immune-immature infants, children, pregnant women, immunocompromised individuals, and immunosenescent individuals aged � years). In addition to the adaptive immune response, there are some data suggesting that trained innate immunity might also have a role in protection against COVID-19. 88 , 89 Multiple clinical trials (eg, <"type":"clinical-trial","attrs":<"text":"NCT04327206","term_id":"NCT04327206">> NCT04327206, <"type":"clinical-trial","attrs":<"text":"NCT04328441","term_id":"NCT04328441">> NCT04328441, <"type":"clinical-trial","attrs":<"text":"NCT04414267","term_id":"NCT04414267">> NCT04414267, and <"type":"clinical-trial","attrs":<"text":"NCT04417335","term_id":"NCT04417335">> NCT04417335) are examining whether unrelated vaccines, such as the measles, mumps, and rubella vaccine and the Bacillus Calmette–Guérin vaccine, can elicit trained innate immunity and confer protection against COVID-19. It is crucial that research focuses on understanding the genetic drivers of infection and vaccine-induced humoral and cellular immunity to SARS-CoV-2, defining detailed targets of humoral and cellular immune responses at the epitope level, characterising the B-cell receptor and T-cell receptor repertoire elicited by infection or vaccination, and establishing the long-term durability, and maintenance, of protective immunity after infection or vaccination. A safe regulatory pathway leading to licensing must also be defined for use of these vaccines in children, pregnant women, immunocompromised people, and nursing home residents. Some have called for further shortening of the vaccine development process through the use of controlled human challenge models. 90 As of Oct 5, 2020, no such studies have occurred, but the UK is considering initiating such trials in early 2021.

Deciphering CD30 ligand biology and its role in humoral immunity

Ligands and receptors in the tumour necrosis factor (TNF) and tumour necrosis factor receptor (TNFR) superfamilies have been the subject of extensive investigation over the past 10-15 years. For certain TNFR family members, such as Fas and CD40, some of the consequences of receptor ligation were predicted before the identification and cloning of their corresponding ligands through in vitro functional studies using agonistic receptor-specific antibodies. For other members of the TNFR family, including CD30, cross-linking the receptor with specific antibodies failed to yield many clues about the functional significance of the relevant ligand-receptor interactions. In many instances, the subsequent availability of TNF family ligands in the form of recombinant protein facilitated the determination of biological consequences of interactions with their relevant receptor in both in vitro and in vivo settings. In the case of CD30 ligand (CD30L CD153), definition of its biological role remained frustratingly elusive. Early functional studies using CD30L+ cells or agonistic CD30-specific antibodies logically focused attention on cell types that had been shown to express CD30, namely certain lymphoid malignancies and subsets of activated T cells. However, it was not immediately clear how the reported activities from these in vitro studies relate to the biological activity of CD30L in the more complex whole animal setting. Recently, results from in vivo models involving CD30 or CD30L gene disruption, CD30L overexpression, or pharmacological blockade of CD30/CD30L interactions have begun to provide clues about the role played by CD30L in immunological processes. In this review we consider the reported biology of CD30L and focus on results from several recent studies that point to an important role for CD30/CD30L interactions in humoral immune responses.


Potential outcomes of CD30L/CD30 interactions…

Potential outcomes of CD30L/CD30 interactions based on published results from in vitro studies.

Are hypotheses based on published…

Are hypotheses based on published in vitro findings predictive of CD30L activity in…


the condition of being immune the protection against infectious disease conferred either by the immune response generated by immunization or previous infection or by other nonimmunologic factors. It encompasses the capacity to distinguish foreign material from self , and to neutralize, eliminate, or metabolize that which is foreign ( nonself ) by the physiologic mechanisms of the immune response.

The mechanisms of immunity are essentially concerned with the body's ability to recognize and dispose of substances which it interprets as foreign and harmful to its well-being. When such a substance enters the body, complex chemical and mechanical activities are set into motion to defend and protect the body's cells and tissues. The foreign substance, usually a protein, is called an antigen , that is, one that generates the production of an antagonist. The most common response to the antigen is the production of antibody . The antigen--antibody reaction is an essential component of the overall immune response. A second type of activity, cellular response, is also an essential component.

The various and complex mechanisms of immunity are basic to the body's ability to protect itself against specific infectious agents and parasites, to accept or reject cells and tissues from other individuals, as in blood transfusions and organ transplants, and to protect against cancer, as when the immune system recognizes malignant cells as not-self and destroys them.

There has been extensive research into the body's ability to differentiate between cells, organisms, and other substances that are self (not alien to the body), and those that are nonself and therefore must be eliminated. A major motivating force behind these research efforts has been the need for more information about growth and proliferation of malignant cells, the inability of certain individuals to develop normal immunological responses (as in immunodeficiency conditions), and mechanisms of failure of the body to recognize its own tissues (as in autoimmune diseases ).

Immunological Responses . Immunological responses in humans can be divided into two broad categories: humoral immunity, which takes place in the body fluids (humors) and is concerned with antibody and complement activities and cell-mediated or cellular immunity, which involves a variety of activities designed to destroy or at least contain cells that are recognized by the body as alien and harmful. Both types of responses are instigated by lymphocytes that originate in the bone marrow as stem cells and later are converted into mature cells having specific properties and functions.

The two kinds of lymphocytes that are important to establishment of immunity are T lymphocytes (T cells) and B lymphocytes (B cells). (See under lymphocyte .) The T lymphocytes differentiate in the thymus and are therefore called thymus-dependent. There are several types involved in cell-mediated immunity, delayed hypersensitivity, production of lymphokines, and the regulation of the immune response of other T and B cells.

The B lymphocytes are so named because they were first identified during research studies involving the immunologic activity of the bursa of Fabricius, a lymphoid organ in the chicken. (Humans have no analogous organ.) They mature into plasma cells that are primarily responsible for forming antibodies, thereby providing humoral immunity.

Humoral Immunity. At the time a substance enters the body and is interpreted as foreign, antibodies are released from plasma cells and enter the body fluids where they can react with the specific antigens for which they were formed. This release of antibodies is stimulated by antigen-specific groups (clones) of B lymphocytes. Each B lymphocyte has IgM immunoglobulin receptors that play a major role in capturing its specific antigen and in launching production of the immunoglobulins (which are antibodies) that are capable of neutralizing and destroying that particular type of antigen.

Most of the B lymphocytes activated by the presence of their specific antigen become plasma cells, which then synthesize and export antibodies. The activated B lymphocytes that do not become plasma cells continue to reside as &ldquomemory&rdquo cells in the lymphoid tissue, where they stand ready for future encounters with antigens that may enter the body. It is these memory cells that provide continued immunity after initial exposure to the antigens.

There are two types of humoral immune response: primary and secondary. The primary response begins immediately after the initial contact with an antigen the resulting antibody appears 48 to 72 hours later. The antibodies produced during this primary response are predominantly of the IgM class of immunoglobulins.

A secondary response occurs within 24 to 48 hours. This reaction produces large quantities of immunoglobulins that are predominantly of the IgG class. The secondary response persists much longer than the primary response and is the result of repeated contact with the antigens. This phenomenon is the basic principle underlying consecutive immunizations .

The ability of the antibody to bind with or &ldquostick to&rdquo antigen renders it capable of destroying the antigen in a number of ways for example, agglutination and opsonization. Antibody also &ldquofixes&rdquo or activates complement , which is the second component of the humoral immune system. Complement is the name given a complex series of enzymatic proteins which are present but inactive in normal serum. When complement fixation takes place, the antigen, antibody, and complement become bound together. The cell membrane of the antigen (which usually is a bacterial cell) then ruptures, resulting in dissolution of the antigen cell and a leakage of its substance into the body fluids. This destructive process is called lysis.

Cellular Immunity. This type of immune response is dependent upon T lymphocytes, which are primarily concerned with a delayed type of immune response. Examples of this include rejection of transplanted organs, defense against slowly developing bacterial diseases that result from intracellular infections, delayed hypersensitivity reactions, certain autoimmune diseases, some allergic reactions, and recognition and rejection of self cells undergoing alteration, for example, those infected with viruses, and cancer cells that have tumor-specific antigens on their surfaces. These responses are called cell-mediated immune responses.

The T lymphocyte becomes sensitized by its first contact with a specific antigen. Subsequent exposure to the antigen stimulates a host of chemical and mechanical activities, all designed to either destroy or inactivate the offending antigen. Some of the sensitized T lymphocytes combine with the antigen to deactivate it, while others set about to destroy the invading organism by direct invasion or the release of chemical factors. These chemical factors, through their influence on macrophages and unsensitized lymphocytes, enhance the effectiveness of the immune response.

Among the more active chemical factors are lymphokines , which are potent and biologically active proteins their names are often descriptive of their functions: Ones that directly affect the macrophages are the macrophage chemotactic factor , which attracts macrophages to the invasion site migration inhibitory factor , which causes macrophages to remain at the invasion site and macrophage-activating factor , which stimulates the metabolic activities of these large cells and thereby improves their ability to ingest the foreign invaders.

Another factor, a protein called interferon , is produced by the body cells, especially T lymphocytes, following viral infection or in response to a wide variety of inducers, such as certain nonviral infectious agents and synthetic polymers.

A portion of the population of T lymphocytes is transformed into killer cells by the lymphocyte-transforming factor (blastogenic factor). These activated lymphocytes produce a lymphotoxin or cytotoxin that damages the cell membranes of the antigens, causing them to rupture.

In order to ensure an ample supply of T lymphocytes, two factors are at work: lymphocyte-transforming factor stimulates lymphocytes that have already undergone conversion to sensitized T lymphocytes, so that they increase their numbers by repeated cell division and clone formation in the absence of antigens, transfer factor takes over the task of sensitizing those lymphocytes that have not been exposed to antigen.

It is apparent that the immune response brings about intensive activity at the site of invasion it is not only the pathogen that is destroyed, but invariably, there is death or damage to some normal tissues.

Interactions Between the Two Systems. There are several areas in which the cellular and humoral systems interact and thereby improve the efficiency of the overall immune response. For example, a by-product of the enzymatic activity of the complement system acts as a chemotactic factor, attracting T lymphocytes and macrophages to the invasion site. In another example, although T lymphocytes are not required for the production of antibody, there is optimal antibody production after interaction between T and B lymphocytes.

For a discussion of abnormalities of the immune response system, see immune response .

Natural immunity is a genetic characteristic of an individual and is due to the particular species and race to which one belongs, to one's sex, and to one's individual ability to produce immune bodies. All humans are immune to certain diseases that affect animals of the lower species males are more resistant to some disorders than are females, and vice versa. Persons of one race are more susceptible to some diseases than those of another race that has had exposure to the infectious agents through successive generations. One's individual ability to produce immune bodies, and thereby ward off pathogens, is influenced by one's state of physical health, one's nutritional status, and one's emotional response to stress.

In order for an individual to acquire immunity one's body must be stimulated to produce its own immune response components (active immunity) or these substances must be produced by other persons or animals and then passed on to the person (passive immunity). Active immunity can be established in two ways: by having the disease or by receiving modified pathogens and toxins. When an individual is exposed to a disease and the pathogenic organisms enter the body, the production of antibody is initiated. After recovery from the illness, memory cells remain in the body and stand ready as a defense against future invasion. It is possible, through the use of vaccines, bacterins, and modified toxins (toxoids), to stimulate the production of specific antibodies without having an attack of the disease. These are artificial means by which an individual can acquire active immunity.

Sometimes it is desirable to provide &ldquoready-made&rdquo immune bodies, as in cases in which the patient has already been exposed to the antigen, is experiencing the symptoms of the disease, and needs reinforcements to help mitigate its harmful effects. Examples of conditions for which an individual may be given such passive immunity include tetanus, diphtheria, and a venomous snake bite. The patient is given immune serum, which contains gamma globulin , antibodies (including antitoxin) produced by the animal from which the serum was taken.

It is not always necessary that the patient actually suffer from the disease and exhibit its symptoms before passive immunity is provided. In some instances in which exposure to an infectious agent is suspected, immune bodies may be given to ward off a full-blown attack or at least to lessen its severity.

Another way in which immunity can be passively acquired is across the placental barrier from fetus to mother. The maternal antibody thus acquired serves as protection for the newborn until he can actively establish immunity on his own. Although humoral immunity can be acquired in this way, cellular immunity cannot.

Watch the video: The Humoral Immune Response - Immunology Animations (October 2022).