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5.6: The Ability to Evade Adaptive Immune Defenses - Biology

5.6: The Ability to Evade Adaptive Immune Defenses - Biology


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Learning Objectives

  1. State four ways the antibody molecules made during adaptive immunity protect us against bacteria.
  2. Briefly describe at least three ways a bacterium might evade our adaptive immune defenses and name a bacterium that does each.

Overview of Adaptive Immune Defenses

One of the major defenses against bacteria is the immune defenses' production of antibody molecules against the organism. The "tips" of the antibody, called the Fab portion (Figure (PageIndex{1})) have shapes that are complementary to portions of bacterial proteins and polysaccharides called epitopes. The "bottom" of the antibody, called the Fc portion (Figure (PageIndex{1})) binds to receptors on phagocytes and NK cells) and can activate the classical complement pathway.

There are various ways that the antibodies the body makes during adaptive immunity protect the body against bacteria:

a. As mentioned above under phagocytosis, some antibodies such as IgG and IgE function as opsonins and stick bacteria to phagocytes (Figure (PageIndex{2})).

b. Antibodies, such as IgG, IgA, and IgM, can bind to bacterial adhesins, pili, and capsules and in this way block their attachment to host cells.

c. IgG and IgM can also activate the classical complement pathway providing all of its associated benefits.

d. IgA and IgM can clump bacteria together enabling them to be more readily removed by phagocytes (Figure (PageIndex{3})).

These mechanisms will be discussed in greater detail in Unit 6.

Exercise: Think-Pair-Share Questions

  1. Staphylococcus aureus produces protein A, a protein that binds to the Fc portion of antibodies.

How might this enable S. aureus to resist adaptive immunity?

  1. Many bacteria that colonize the mucous membranes produce immunoglobulin protease, an enzyme that hydrolizes antibodies of the IgA class.

How might this enable these bacteria to resist adaptive immunity?

Resisting Adaptive Immune Defenses

Bacteria utilize a variety of mechanisms to resist antibodies made during adaptive immunity. These include the following:

a. Certain bacteria can evade antibodies is by changing the adhesive tips of their pili as mentioned above with Escherichia coli and Neisseria gonorrhoeae (Figure (PageIndex{4})).

Bacteria can also vary other surface proteins so that antibodies previously made against those proteins will no longer "fit." (Figure (PageIndex{5})). For example, N. gonorrhoeae produces Rmp protein (protein III) that protects against antibody attack by antibodies made against other surface proteins (such as adhesins) and the lipooligosaccharide (LOS) of the bacterium.

b. Strains of Neisseria meningitidis have a capsule composed of sialic acid while strains of Streptococcus pyogenes (group A beta streptococci) have a capsule made of hyaluronic acid. Both of these polysaccharides closely resemble carbohydrates found in human tissue and because they are not recognized as foreign by the lymphocytes that carry out the adaptive immune responses, antibodies are not made against those capsules. Likewise, some bacteria are able to coat themselves with host proteins such as fibronectin, lactoferrin, or transferrin and in this way avoid having antibodies being made against them because they are unable to be recognized as foreign by lymphocytes.

c. Staphylococcus aureus produces protein A while Streptococcus pyogenes produces protein G. Both of these proteins bind to the Fc portion of the antibody IgG, the portion that is supposed to bind the bacterium to phagocytes during enhanced attachment (Figure (PageIndex{1})). The bacteria become coated with antibodies in a way that does not result in opsonization (Figure (PageIndex{6})).

d. Salmonella species can undergo phase variation of their capsular (K) and flagellar (H) antigens, that is, they can change the molecular shape of their capsular and flagellar antigens so that antibodies made against the previous form no longer fit the new form (Figure (PageIndex{5})).

e. Bacteria such as Haemophilus influenzae, Streptococcus pneumoniae, Helicobacter pylori, Shigella flexneri, Neisseria meningitidis, Neisseria gonorrhoeae and enteropathogenic E. coli produce immunoglobulin proteases. Immunoglobulin proteases degrade the body's protective antibodies (immunoglobulins) that are found in body secretions, a class of antibodies known as IgA.

f. Many pathogenic bacteria, as well as normal flora, form complex bacterial communities as biofilms. Bacteria in biofilms are often able to communicate with one another by a process called quorum sensing (discussed later in this unit) and are able to interact with and adapt to their environment as a population of bacteria rather than as individual bacteria. By living as a community of bacteria as a biofilm, these bacteria are better able to resist attack by antibiotics and are better able to resist the host immune system.

Summary

  1. There are various ways that the antibodies the body makes during adaptive immunity protect the body against bacteria.
  2. Some antibodies such as IgG and IgE function as opsonins and stick bacteria to phagocytes (opsonization or enhanced attachment).
  3. Antibodies, such as IgG, IgA, and IgM, can bind to bacterial adhesins, pili, and capsules and in this way block their attachment to host cells.
  4. IgG and IgM can activate the classical complement pathway providing all of its associated benefits.
  5. IgA and IgM can clump bacteria together enabling them to be more readily removed by phagocytes.
  6. Antitoxin antibodies, mainly IgG, are made against bacterial exotoxins. They combine with the exotoxin molecules before they can interact with host target cells and thus neutralize the toxin.
  7. Bacteria utilize a variety of mechanisms to resist antibodies made during adaptive immunity.
  8. Some bacteria can vary their surface proteins or polysaccharides so that antibodies previously made against those proteins will no longer "fit."
  9. Some bacteria are able to coat themselves with host proteins and in this way avoid having antibodies being made against them because they are unable to be recognized as foreign
  10. Some bacteria produce immunoglobulin proteases that degrade the body's protective antibodies (immunoglobulins) that are found in body secretions.

How kids’ immune systems can evade COVID

Young children account for only a small percentage of COVID-19 infections 1 — a trend that has puzzled scientists. Now, a growing body of evidence suggests why: kids’ immune systems seem better equipped to eliminate SARS-CoV-2 than are adults’.

“Children are very much adapted to respond — and very well equipped to respond — to new viruses,” says Donna Farber, an immunologist at Columbia University in New York City. Even when they are infected with SARS-CoV-2, children are most likely to experience mild or asymptomatic illness 2 .

Another clue that children’s response to the virus differs from that of adults is that some children develop COVID-19 symptoms and antibodies specific to SARS-CoV-2 but never test positive for the virus on a standard RT-PCR test. In one study, three children under ten from the same family developed SARS-CoV-2 antibodies 3 — and two of them even experienced mild symptoms — but none tested positive on RT-PCR, despite being tested 11 times over 28 days while in close contact with their parents, who had tested positive.


B and T Cells

Lymphocytes, which are a subclass of white blood cells, are formed with other blood cells in the red bone marrow found in many flat bones, such as the shoulder or pelvic bones. The two types of lymphocytes of the adaptive immune response are B and T cells (Figure 1). Whether an immature lymphocyte becomes a B cell or T cell depends on where in the body it matures. The B cells remain in the bone marrow to mature (hence the name “B” for “bone marrow”), while T cells migrate to the thymus, where they mature (hence the name “T” for “thymus”). During the maturation process, each B or T cell develops unique surface proteins that are able to recognize a unique set of very specific molecules on antigens (discussed below). In other words, each B or T cell can recognize only a very few different molecules, but together the entire lymphocyte population in a healthy person should be able to recognize molecules from most pathogens. The specificity of these unique surface proteins, or receptors, on the lymphocytes is determined by the genetics of the individual and is present before a foreign molecule is introduced to the body or encountered. Except in certain immune system diseases called autoimmune diseases, no mature B or T cells are able to recognize and bind to molecules that are found on healthy human cells, but only to molecules found on pathogens or on unhealthy human cells.

B cells are involved in the humoral immune response, which targets pathogens loose in blood and lymph, and B cells carry out this response by secreting antibodies.T cells are involved in the cell-mediated immune response, which targets infected cells in the body. T cells include the Helper T cells and the Cytotoxic, or Killer, T cells. Cytotoxic T cells directly kill human cells that are infected or unhealthy. Helper T cells do not directly kill infected cells, but secrete molecules that are crucial for the function of all other cells in the immune response to a pathogen.

Figure 1. This scanning electron micrograph shows a T lymphocyte. T and B cells are indistinguishable by light microscopy but can be differentiated experimentally by probing their surface receptors. (credit: modification of work by NCI scale-bar data from Matt Russell)


Adaptive Immune System

The adaptive immune system is activated if pathogens successfully enter the body and manage to evade the general defenses of the innate immune system. An adaptive response is specific to the particular type of pathogen that has invaded the body, or to cancerous cells. It takes longer to launch a specific attack, but once it is underway, its specificity makes it very effective. An adaptive response also usually leads to immunity. This is a state of resistance to a specific pathogen, due to the adaptive immune system’s ability to “remember” the pathogen and immediately mount a strong attack tailored to that particular pathogen if it invades again in the future.


Chapter 17 Summary

In this chapter, you learned about the immune system. Specifically, you learned that:

  • Any agent that can cause disease is called a pathogen . Most human pathogens are microorganisms , such as bacteria and viruses . The immune system is the body system that defends the human host from pathogens and cancerous cells.
  • The innate immune system is a subset of the immune system that provides very quick, but non-specific responses to pathogens. It includes multiple types of barriers to pathogens, leukocytes that phagocytize pathogens, and several other general responses.
  • The adaptive immune system is a subset of the immune system that provides specific responses tailored to particular pathogens. It takes longer to put into effect, but it may lead to immunity to the pathogens.
  • Both innate and adaptive immune responses depend on the ability of the immune system to distinguish between self and non-self molecules. Most body cells have major histocompatibility complex (MHC) proteins that identify them as self. Pathogens, infected cells, and tumor cells have non-self proteins called antigens that the immune system recognizes as foreign.
  • Antigens are proteins that bind to specific receptors on immune system cells and elicit an adaptive immune response. Some immune cells ( B cells ) respond to foreign antigens by producing antibodies that bind with antigens and target pathogens for destruction.
  • An important role of the immune system is tumor surveillance. Killer T cells of the adaptive immune system find and destroy tumor cells, which they can identify from their abnormal antigens.
  • The neuroimmune system that protects the central nervous system is thought to be distinct from the peripheral immune system that protects the rest of the human body. The blood-brain and blood-spinal cord barriers are one type of protection of the neuroimmune system. Neuroglia also play a role in this system, for example, by carrying out phagocytosis .
  • The lymphatic system is a human organ system that is a vital part of the adaptive immune system. It consists of several organs and a system of vessels that transport or filter the fluid called lymph . The main immune function of the lymphatic system is to produce, mature, harbor, and circulate white blood cells called lymphocytes, which are the main cells in the adaptive immune system, and are circulated in lymph.
    • The return of lymph to the bloodstream is one of the functions of the lymphatic system. Lymph flows from tissue spaces, where it leaks out of blood vessels, to major veins in the upper chest. It is then returned to the cardiovascular system . Lymph is similar in composition to blood plasma . Its main cellular components are lymphocytes.
    • Lymphatic vessels called lacteals are found in villi that line the small intestine . Lacteals absorb fatty acids from the digestion of lipids in the digestive system . The fatty acids are then transported through the network of lymphatic vessels to the bloodstream.
    • Lymphocytes, which include B cells and T cells , are the subset of leukocytes involved in adaptive immune responses . They may create a lasting memory of and immunity to specific pathogens.
    • All lymphocytes are produced in bone marrow and then go through a process of maturation, in which they “learn” to distinguish self from non-self. B cells mature in the bone marrow, and T cells mature in the thymus . Both the bone marrow and thymus are considered primary lymphatic organs .
    • Secondary lymphatic organs include the tonsils, spleen, and lymph nodes. There are four pairs of tonsils that encircle the throat. The spleen filters blood, as well as lymph. There are hundreds of lymph nodes located in clusters along the lymphatic vessels. All of these secondary organs filter lymph and store lymphocytes, so they are sites where pathogens encounter and activate lymphocytes and initiate adaptive immune responses.
      • The body’s first line of defense consists of three different types of barriers that keep most pathogens out of body tissues. The types of barriers are mechanical, chemical, and biological barriers.
          • Mechanical barriers — which include the skin , mucous membranes , and fluids (such as tears and urine ) — physically block pathogens from entering the body.
          • Chemical barriers — such as enzymes in sweat , saliva , and semen — kill pathogens on body surfaces.
          • Biological barriers are harmless bacteria that use up food and space so pathogenic bacteria cannot colonize the body.
            • Most activated T cells become either killer T cells or helper T cells . Killer T cells destroy cells that are infected with pathogens or are cancerous. Helper T cells manage immune responses by releasing cytokines that control other types of leukocytes.
            • Activated B cells form plasma cell s that secrete antibodies, which bind to specific antigens on pathogens or infected cells. The antibody-antigen complexes generally lead to the destruction of the cells, for example, by attracting phagocytes or triggering the complement system.
              • Active immunity occurs when the immune system has been presented with antigens that elicit an adaptive immune response. This may occur naturally as the result of an infection, or artificially as the result of immunization. Active immunity may last for years or even for life.
              • Passive immunity occurs without an adaptive immune response by the transfer of antibodies or activated T cells. This may occur naturally between a mother and her fetus or her nursing infant, or it may occur artificially by injection. Passive immunity lasts only as long as the antibodies or activated T cells remain alive in the body, generally just weeks or months.
                • The prevalence of allergies has been increasing for decades, especially in developed countries, where they are much more common than in developing countries. The hygiene hypothesis posits that this has occurred because humans evolved to cope with more pathogens than we now typically face in our relatively sterile environments in developed countries. As a result, the immune system “keeps busy” by attacking harmless antigens.
                • Allergies occur when B cells are first activated to produce large amounts of antibodies to an otherwise harmless allergen, and the antibodies attach to mast cells. On subsequent exposures to the allergen, the mast cells immediately release cytokines and histamines that cause inflammation.
                • Mild allergy symptoms are frequently treated with antihistamines that counter histamines and reduce allergy symptoms. A severe systemic allergic reaction, called anaphylaxis , is a medical emergency that is usually treated with injections of epinephrine. Immunotherapy for allergies involves injecting increasing amounts of allergens to desensitize the immune system to them.
                  • In some autoimmune diseases, such as type I diabetes, the immune system attacks and damages specific body cells. In other autoimmune diseases, such as systemic lupus erythematosus, many different tissues and organs may be attacked and injured. Autoimmune diseases generally cannot be cured, but their symptoms can often be managed with drugs or other treatments.
                    • Primary immunodeficiency is present at birth and caused by rare genetic diseases. An example is severe combined immunodeficiency. Secondary immunodeficiency occurs because of some event or exposure experienced after birth. Possible causes include substance abuse, obesity, and malnutrition, among others.
                    • The most common cause of immunodeficiency in the world today is human immunodeficiency virus (HIV), which infects and destroys helper T cells. HIV is transmitted through mucous membranes or body fluids. The virus may eventually lead to such low levels of helper T cells that opportunistic infections occur. When this happens, the patient is diagnosed with acquired immunodeficiency syndrome (AIDS). Medications can control the multiplication of HIV in the human body, but it can’t eliminate the virus completely.

                    Up to this point, this book has covered body systems that carry out processes within individuals, such as the digestive, muscular, and immune systems. Read the next chapter to learn about the body system that allows humans to produce new individuals — the reproductive system.


                    11-4. Immunosuppression or inappropriate immune responses can contribute to persistent disease

                    Many pathogens suppress immune responses in general. For example, staphylococci produce toxins, such as the staphylococcal enterotoxins and toxic shock syndrome toxin-1 ( Toxic Shock Syndrome, in Case Studies in Immunology, see Preface for details), that act as superantigens. Superantigens are proteins that bind the antigen receptors of very large numbers of T cells (see Section 7-26), stimulating them to produce cytokines that cause significant suppression of all immune responses. The details of this suppression are not understood. The stimulated T cells proliferate and then rapidly undergo apoptosis, leaving a generalized immunosuppression together with the deletion of many peripheral T cells.

                    Many other pathogens cause mild or transient immunosuppression during acute infection. These forms of suppressed immunity are poorly understood but important, as they often make the host susceptible to secondary infections by common environmental microorganisms. A crucially important example of immune suppression follows trauma, burns, or even major surgery. The burned patient has a clearly diminished capability to respond to infection, and generalized infection is a common cause of death in these patients. The reasons for this are not fully understood.

                    Measles virus infection, in spite of the widespread availability of an effective vaccine, still accounts for 10% of the global mortality of children under 5 years old and is the eighth leading cause of death worldwide. Malnourished children are the main victims and the cause of death is usually secondary bacterial infection, particularly pneumonia caused by measles-induced immunosuppression. The immunosuppression that follows measles infection can last for several months and is associated with reduced T- and B-cell function. There is reduced or absent delayed-type hypersensitivity and, during this period of acquired immunodeficiency, children have markedly increased susceptibility to mycobacterial infection, reflecting the important role of macrophage activation by TH1 cells in host defense against mycobacteria. An important mechanism for measles-induced immunosuppression is the infection of dendritic cells by measles virus. Infected dendritic cells cause unresponsiveness of T lymphocytes by mechanisms that are not yet understood, and it seems likely that this is the proximate cause of the immunosuppression induced by measles virus.

                    The most extreme case of immune suppression caused by a pathogen is the acquired immune deficiency syndrome caused by infection with HIV. The ultimate cause of death in AIDS is usually infection with an opportunistic pathogen, a term used to describe a microorganism that is present in the environment but does not usually cause disease because it is well controlled by normal host defenses. HIV infection leads to a gradual loss of immune competence, allowing infection with organisms that are not normally pathogenic.

                    Leprosy, which we discussed in Section 8-13, is a more complex case, in which the causal bacterium, Mycobacterium leprae, is associated either with the suppression of cell-mediated immunity or with a strong cell-mediated antibacterial response. This leads to two major forms of the disease—lepromatous and tuberculoid leprosy. In lepromatous leprosy, cell-mediated immunity is profoundly depressed, M. leprae are present in great profusion, and cellular immune responses to many antigens are suppressed. This leads to a phenotypic state in such patients called anergy, here meaning the absence of delayed-type hypersensitivity to a wide range of antigens unrelated to M. leprae. In tuberculoid leprosy, by contrast, there is potent cell-mediated immunity with macrophage activation, which controls but does not eradicate infection. Few viable microorganisms are found in tissues, the patients usually survive, and most of the symptoms and pathology are caused by the inflammatory response to these persistent microorganisms (Fig. 11.6). The difference between the two forms of disease might lie in a difference in the ratio of TH1 to TH2 cells, and this is thought to be caused by cytokines produced by CD8 T cells, as we learned in Section 10-6.

                    Figure 11.6

                    T-cell and macrophage responses to Mycobacterium leprae are sharply different in the two polar forms of leprosy. Infection with M. leprae, which stain as small dark red dots in the photographs, can lead to two very different forms of disease. In tuberculoid (more. )


                    Virus-Induced Immunopathology

                    A host clearly has numerous mechanisms to recognize and eliminate the viruses that it encounters. However, some viruses persist despite these mechanisms, and then the immune responses may become detrimental to the host and cause immune-mediated disease. When an antigen (virus) persists, pathologic changes and diseases result from different types of immunologic interactions, including immediate hypersensitivity, antibody-mediated immune complex syndrome, and tissue damage caused by cell-mediated effector cells and antibody plus complement. Of these mechanisms, the immune complex syndrome during viral infections has been studied most intensively. Two major complications of deposition of immune complexes are vascular damage and nephritis. Some viral diseases in which immune complexes have been demonstrated are hepatitis B, infectious mononucleosis, dengue hemorrhagic fever, and subacute sclerosing panencephalitis.

                    Cytotoxic T cells also mediate immunopathologic injury in murine models of human infections (i.e., infections with lymphocytic choriomeningitis virus and poxviruses). Both cytotoxic T cells and T cells responsible for delayed-type hypersensitivity have also been implicated in the pathology associated with influenza pneumonia and coxsackievirus myocarditis of mice. A delicate balance between the removal of infected cells that are the source of viral progeny and injury to vital cells probably exists for T cells as well as for the other host immune components.

                    Viruses may sometimes circumvent host defenses. An important factor that may impair the function of sensitized T lymphocytes is apparent from the observation that T cells activated by reaction with antigen or mitogen lose their normal resistance to many viruses. Therefore, these activated T lymphocytes develop the capacity to support the replication of viruses, leading to impairment of T lymphocyte function.


                    Viruses Can Have Immune System, Study Finds

                    A new research led by Dr Kimberley Seed from the Tufts University School of Medicine provides the first evidence that bacteriophages – viruses that infect and replicate within bacteria – can acquire a wholly functional and adaptive immune system.

                    Electron micrograph of bacteriophages infecting a bacterial cell (Dr Graham Beards)

                    The study, published today in the journal Nature, finds that a viral predator of the cholera bacteria can steal the functional immune system of bacteria and use it against its bacterial host. The bacteriophage (phage for short) used the stolen immune system to disable – and thus overcome – the cholera bacteria’s defense system against phages. Therefore, the phage can kill the cholera bacteria and multiply to produce more phage offspring, which can then kill more cholera bacteria.

                    The discovery has dramatic implications for phage therapy, which is the use of phages to treat bacterial diseases. Developing phage therapy is particularly important because some bacteria, called superbugs, are resistant to most or all current antibiotics.

                    Until now, scientists thought phages existed only as primitive particles of DNA or RNA and therefore lacked the sophistication of an adaptive immune system, which is a system that can respond rapidly to a nearly infinite variety of new challenges. Phages are viruses that prey exclusively on bacteria and each phage is parasitically mated to a specific type of bacteria. This study focused on a phage that attacks Vibrio cholerae, the bacterium responsible for cholera epidemics in humans.

                    The researchers used phage lacking the adaptive immune system to infect a new strain of cholera bacteria that is naturally resistant to the phage. The phage was unable to adapt to and kill the cholera strain. They next infected the same strain of cholera bacteria with phage harboring the immune system, and observed that the phage rapidly adapted and thus gained the ability to kill the cholera bacteria. This work demonstrates that the immune system harbored by the phage is fully functional and adaptive.

                    Bacteriophage structure (Adenosine / Pbroks13 / CC BY-SA 2.5)

                    “Virtually all bacteria can be infected by phages. About half of the world’s known bacteria have this adaptive immune system, called CRISPR/Cas, which is used primarily to provide immunity against phages. Although this immune system was commandeered by the phage, its origin remains unknown because the cholera bacterium itself currently lacks this system. What is really remarkable is that the immune system is being used by the phage to adapt to and overcome the defense systems of the cholera bacteria. Finding a CRISPR/Cas system in a phage shows that there is gene flow between the phage and bacteria even for something as large and complex as the genes for an adaptive immune system,” Dr Seed said.

                    “The study lends credence to the controversial idea that viruses are living creatures, and bolsters the possibility of using phage therapy to treat bacterial infections, especially those that are resistant to antibiotic treatment,” added senior author Prof Andrew Camilli, also from the Tufts University School of Medicine.

                    Bibliographic information: Seed KD et al. 2013. A bacteriophage encodes its own CRISPR/Cas adaptive response to evade host innate immunity. Nature, vol. 494, no. 7438, pp. 489–491 doi: 10.1038/nature11927


                    Immunological Memory Is Due to Both Clonal Expansion and Lymphocyte Differentiation

                    The adaptive immune system, like the nervous system, can remember prior experiences. This is why we develop lifelong immunity to many common infectious diseases after our initial exposure to the pathogen, and it is why vaccination works. The same phenomenon can be demonstrated in experimental animals. If an animal is immunized once with antigen A, an immune response (either antibody or cell-mediated) appears after several days, rises rapidly and exponentially, and then, more gradually, declines. This is the characteristic course of a primary immune response, occurring on an animal's first exposure to an antigen. If, after some weeks, months, or even years have elapsed, the animal is reinjected with antigen A, it will usually produce a secondary immune response that is very different from the primary response: the lag period is shorter, and the response is greater. These differences indicate that the animal has “remembered” its first exposure to antigen A. If the animal is given a different antigen (for example, antigen B) instead of a second injection of antigen A, the response is typical of a primary, and not a secondary, immune response. The secondary response must therefore reflect antigen-specific immunological memory for antigen A (Figure 24-10).

                    Figure 24-10

                    Primary and secondary antibody responses. The secondary response induced by a second exposure to antigen A is faster and greater than the primary response and is specific for A, indicating that the adaptive immune system has specifically remembered encountering (more. )

                    The clonal selection theory provides a useful conceptual framework for understanding the cellular basis of immunological memory. In an adult animal, the peripheral lymphoid organs contain a mixture of cells in at least three stages of maturation: naïve cells, effector cells and memory cells. When naïve cells encounter antigen for the first time, some of them are stimulated to proliferate and differentiate into effector cells, which are actively engaged in making a response (effector B cells secrete antibody, while effector T cells kill infected cells or help other cells fight the infection). Instead of becoming effector cells, some naïve cells are stimulated to multiply and differentiate into memory cells�lls that are not themselves engaged in a response but are more easily and more quickly induced to become effector cells by a later encounter with the same antigen. Memory cells, like naïve cells, give rise to either effector cells or more memory cells (Figure 24-11).

                    Figure 24-11

                    A model for the cellular basis of immunological memory. When naïve lymphocytes are stimulated by their specific antigen, they proliferate and differentiate. Most become effector cells which function and then die, while others become long-lived (more. )

                    Thus, immunological memory is generated during the primary response in part because the proliferation of antigen-stimulated naïve cells creates many memory cells𠅊 process known as clonal expansion𠅊nd in part because memory cells are able to respond more sensitively and rapidly to the same antigen than do naïve cells. And, unlike most effector cells, which die within days or weeks, memory cells can live for the lifetime of the animal, thereby providing lifelong immunological memory.


                    5.6: The Ability to Evade Adaptive Immune Defenses - Biology

                    HIV is stopped by innate defenses. HIV cannot penetrate unbroken skin. HIV is transmitted through direct exchange of body fluids. Sexual intercourse is the most common mode of transmission. Blood to blood contact, such as through sharing needles for intravenous injection or blood transfusion can also transmit HIV. Infected mothers can pass HIV to their infants during pregnancy, birth and breastfeeding.

                    HIV transmitted through sexual activity enters the bloodstream via mucous membranes lining the vagina, rectum and mouth. Macrophages and dendritic cells on the surface of mucous membranes bind virus and shuttle it into the lymph nodes, which contain high concentrations of helper T cells (CD4+ T cells).

                    Once HIV has entered the body, the immune system initiates anti-HIV antibody and cytotoxic T cell production. However, it can take one to six months for an individual exposed to HIV to produce measurable quantities of antibody. The immune response is weakened as memory T cells (CD4 + CCR5 + ) are destroyed.

                    The figure shows a scanning EM picture of a dendritic cell interacting with helper T cells. This process occurs in lymph nodes and regulates immune responses.

                    Copyright � Massachusetts Medical Society. All rights reserved. Used and adapted with permission.
                    New England Journal of Medicine 340:1732


                    Watch the video: The Immune System: Innate Defenses and Adaptive Defenses (May 2022).