Prescott’s Microbiology, 9th Edition
34
Adaptive Immunity
CHAPTER OVERVIEW
This chapter focuses on specific (adaptive) immunity, a complex process involving interactions of the antigens
of a pathogen with antigen-receptors and antibodies of a host. These interactions trigger a series of events that
either destroy the pathogen or render it harmless. Most of the chapter is devoted to discussions of the
functional cells and molecules of the specific immune system. During the discussion, the various connections
between these cells and molecules are drawn and linked to other types of immune responses. The chapter
continues with a discussion of the ways these responses protect higher animals against viral and bacterial
pathogens. It concludes with a discussion of hypersensitivities (allergies), autoimmune diseases, and
immunodeficiencies.
LEARNING OUTCOMES
After reading this chapter you should be able to:
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contrast host innate resistance with adaptive immunity
outline the localization of B and T cells during development
predict the types of molecules that can serve as antigens
compare haptens and true antigens
report the methods by which immunity occurs by natural and artificial means
distinguish between the active and passive forms of natural and artificial immunity
define the method by which a host distinguishes itself from nonself (foreign) materials
diagram the host cell receptors that distinguish self from nonself
compare the processes by which MHC class I and class II receptors recognize foreignness
identify cells that can function as antigen-presenting cells (APCs)
explain the use of “cluster of differentiation” (CD) molecules to name cells
categorize T cells based on their CD designation
contrast the biological functions of T-cell subsets
describe T-cell receptor structure and function
illustrate the T-cell developmental process
connect antigen presentation within MHC receptors and T-cell subset recognition
build a model of the molecular events resulting in T-cell activation
describe the B-cell receptor structure and function
illustrate the B-cell maturation process in response to antigen triggering
compare T-dependent and T-independent B-cell activation
build a model of the molecular events resulting in B-cell activation
describe the structure of the B-cell receptor that is secreted as antibody
compare and contrast the five classes of antibody
diagram the antibody changes, induced by antigen binding, that facilitate antigen capture and removal
from the host
integrate antibody secretion with antigen exposure
create a model of genetic diversity that results from recombination, alternative splicing, and somatic
hypermutation
predict antibody specificity resulting from clonal selection
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Prescott’s Microbiology, 9th Edition
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explain the consequences of antibody binding of antigen
assess the effectiveness of antigen removal by antibody
predict which antigens will be most susceptible to antibody action
evaluate the impact of improper B-cell activation
contrast the outcome of B-cell and T-cell exposure to self antigens
illustrate differences between hypersensitivity, autoimmunity, tissue rejection, and immunodeficiency
relate types of hypersensitivity to the root biological cause
predict disease potential due to the presence in the body of “self-reactive” T and B cells
explain tissue rejection as a function of cells responding to the graft
propose the impact on immunity when T cells and B cells become deficient
CHAPTER OUTLINE
I.
Overview of Adaptive Immunity
A. Specific immune system
1. Has three major functions
a. Recognize anything that is nonself
b. Respond to this foreign material (effector response)—involves the recruitment of various
defense molecules and cells to either destroy foreign material or render it harmless
c. Remember the foreign invader (anamnestic response)—a more rapid and intense
response to foreign material that occurs upon later encounters with that material
2. The characteristics of specificity and memory distinguish the specific immune response from
nonspecific resistance
3. There are two arms of specific immunity
a. Humoral (antibody-mediated) immunity—based on action of antibodies that bind
bacteria, toxins, and extracellular viruses, tagging or marking them for destruction
b. Cellular (cell-mediated) immunity—based on action of T cells that directly attack cells
infected with viruses or parasites, transplanted cells or organs, and cancer cells
II. Antigens
A. Prior to birth, the immune system removes most T cells specific for self-recognition determinants, to
focus the immune response on antigens
B. Antigens are substances, such as proteins, nucleoproteins, polysaccharides, and some glycolipids
that elicit an immune response and react with products of that response
1. Epitopes (antigenic determinant sites) are areas of an antigen that can stimulate production of
specific antibodies and that can combine with them
2. Valence—the number of epitopes on an antigen; determines number of antibody molecules an
antigen can combine with at one time
3. Antibodies have two antigen-binding sites and can cross-link multivalent antigens, causing
agglutination (precipitation)
C. Haptens—a small organic molecule that is not itself antigenic but that may become antigenic when
bound to a larger carrier molecule
III. Types of Adaptive Immunity
A. Acquired immunity develops after exposure to antigen or after transfer of antibodies or lymphocytes
from an immune donor
B. Naturally acquired immunity
1. Naturally acquired active immunity—an individual comes in contact with an antigen via a
natural process (e.g., infection) and produces sensitized lymphocytes and/or antibodies that
inactivate or destroy the antigen
2. Naturally acquired passive immunity—transfer (e.g., transplacentally or in breast milk) of
antibodies from one individual (where they were actively produced) to another (where they are
passively received)
C. Artificially acquired immunity
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Prescott’s Microbiology, 9th Edition
1.
Artificially acquired active immunity—deliberate exposure of an individual to a vaccine (a
solution containing antigen) with subsequent development of an immune response
2. Artificially acquired passive immunity—deliberate introduction of antibodies from an immune
donor into an individual
IV. Recognition of Foreignness
A. The immune system must be able to distinguish between resident (self) and foreign (nonself) cells
B. Major histocompatability complex (MHC) is a group of genes that encode three classes of proteins;
only class I and class II are involved in antigen presentation; called human leukocyte antigen (HLA)
complex in humans and H-2 complex in mice
1. Each person has two sets of MHC genes that are codominant; more closely related individuals
have more closely related MHC genes
2. Class I and II MHC
a. Both class I and class II MHC molecules consist of two protein chains and are
transmembrane proteins in the plasma membrane
b. Both class I and class II MHC molecules fold into similar shapes, each having a deep
groove into which a short peptide or other antigen fragment can bind
c. The presence of a foreign peptide in this groove alerts the immune system and activates T
cells or macrophages
d. For class I molecules, the peptides are produced intracellularly (e.g., from replicating
viruses) by antigen processing in the proteosome; proteins pumped from cytoplasm to
endoplasmic reticulum, where they become associated with newly synthesized class I
MHC molecules; the peptide-class I MHC complex is then carried to and incorporated
into the plasma membrane; detected by cytotoxic T cells
e. For class II molecules, exocytosis brings antigens into antigen-presenting cells (APCs)
and produces fragments in phagolysosomes; these peptides combine with class II MHC
and are delivered to cell surface; detected by T-helper cells
C. Cluster of differentiation molecules (CDs)—functional cell surface proteins that are used to
differentiate leukocyte subpopulations; concentration of these molecules in serum is usually low and
elevated levels are associated with disease (e.g., various cancers, autoimmune diseases, HIV
infection); levels in serum can be used in disease management
V. T-Cell Biology
A. T-cell receptors—bind to antigens only when an antigen-presenting cell presents antigen
B. T-cell activation—require two signals for activation: presentation of antigen by an antigenpresenting cell and binding of a T H receptor to a macrophage surface protein
C. Types of T cells
1. T cells originate from CD34+ stem cells in the bone marrow that migrate to the thymus for
further differentiation; the cells are activated by antigen-MHC, proliferate, and form effector
and memory cells
2. T-helper cells (TH or CD4+ cells)
a. TH0—undifferentiated precursors to T H1, TH2, and TH17 cells
b. TH1, TH2, and TH17 cells—each produce and secrete a specific mixture of cytokines
c. TH1 cells promote cytotoxic T cell activity, activate macrophages, and mediate
inflammation and type IV hypersensitivities
d. TH2 cells stimulate antibody responses in general and defend against helminths
e. TH17 cells respond to bacterial invasion with defensins, recruitment of neutrophils, and
inducing inflammation
f.
T-helper cells activate B cells for antibody production; follicular helper T cells (TFH)
seem important to this function
g. Regulatory T cells (Tregs) – exert suppressor regulatory functions by secreting
interleukins
h. Follicular helper T cells (TFH)- Assist in migration of B cells to lymph node follicles.
3. Cytotoxic T cells (CTLs or CD8+ T cells) attach by their T-cell receptor to virus-infected cells
that display class I MHC proteins and viral antigens; are then stimulated by T-helper cells;
activated cytotoxic T cells produce cytokines that limit viral reproduction and activate
macrophages and other phagocytic cells; ultimately cytotoxic T cell destroys target cell; two
mechanisms are:
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Prescott’s Microbiology, 9th Edition
a.
CD95 pathway—transmembrane signal transduction leads to initiation of apoptosis;
CD95 is encoded by a member of the tumor necrosis factor family of genes
b. Perforin pathway—release of perforins that damage the target cell membrane, resulting in
cytolysis of target cell
4. Regulatory T cells prevent recognition of self antigens by other T cells and inhibit T H1 and
TH17 cells from upregulating inflammation
D. Superantigens—bacterial proteins that provoke a dramatic immune response by nonspecifically
stimulating T cells to proliferate; T-cell proliferation occurs when superantigen interacts both with
class II MHC molecules and T-cell receptors; this leads to release of massive quantities of
cytokines, which can cause disease symptoms; superantigens are associated with various chronic
diseases including rabies, staphylococcal food poisoning, and others
VI. B-Cell Biology
A. Have surface molecules important to their function
1. Surface molecules include B-cell receptors (BCRs—IgM and IgD on surface of B cell), Fc
receptors, and complement receptors
2. Binding of receptors to target molecules is involved in activation of B cell and in
phagocytosis, processing, and presentation of antigens
3. Mature B cells are specific for a single antigen epitope with the population of B cells able to
recognize 1013 different epitopes
4. Upon activation, B cells differentiate into plasma cells and memory cells; they also can act as
antigen-presenting cells
B. B-cell activation
1. T-dependent antigen-triggering-B cells specific for an epitope cannot develop into plasma cells
without collaboration with helper T cells
a. The APC presents antigen in its class II MHC to the helper T cell
b. Helper T cells directly associate with B cells that display the same antigen-MHC
complex as presented on the APC
c. The B cell also requires the antigen, recognized through its BCR, to help trigger the
response
d. Additional cytokines are released and the B cells proliferate, differentiate into plasma
cells, and produce antibodies
2. T-independent antigen triggering
a. Polymeric antigens have a large number of identical epitopes that can crosslink BCRs
and cause cell activation; the antibodies produced have low affinity for antigen; no
memory cells are produced
3.
Microbial Pattern Triggering - subset of B cells can respond to induction by toll-like receptor
ligands. Now called innate response activator (IRA)B cells may be responsible for the
immune system’s acute response to gram negative bacteria and LPS.
VII. Antibodies
A. Antibody (immunoglobulin, Ig)—glycoproteins of the immune system that fall into five different
classes: IgG, IgA, IgM, IgD, and IgE
B. Immunoglobulin structure
1. Multiple antigen-combining sites (usually two; some can form multimeric antibodies with up
to 10 combining sites)
2. Basic structure is composed of four polypeptide chains
a. There are two heavy chains and two light chains
b. Within each chain are a constant region (little amino acid sequence variation within the
same class of Ig) and a variable region
3. The four polypeptides are arranged in the form of a flexible Y
a. Fc (crystallizable fragment) is stalk of the Y; contains site at which antibody can bind to a
cell; composed only of constant region
b. Fab (antigen-binding fragments) are at the top of the Y; they bind compatible epitopes of
an antigen; composed of both constant and variable regions
c. Domains—homologous units, each about 100 amino acids long, observed in heavy chains
and in light chains
4. Light chain exists in two distinct forms kappa () and lambda ()
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Prescott’s Microbiology, 9th Edition
5.
C.
D.
E.
There are five types of heavy chains: gamma (), alpha (), mu (), delta (), and epsilon ();
these determine, respectively, the five classes (isotypes) of immunoglobulins: IgG, IgA, IgM,
IgD, and IgE
Immunoglobulin function
1. Fab region binds to antigen whereas Fc region mediates binding to host tissue, various cells of
the immune system, some phagocytic cells, or the first component of the complement system
2. Binding of antibody to an antigen does not destroy the antigen, but marks (targets) the antigen
for immunological attack and activates nonspecific immune responses that destroy the antigen
3. Antigen-antibody binding occurs within the pocket formed by folding the V H and VL regions
of Fab; binding is due to weak, noncovalent bonds and, in most cases, shapes of epitope and
binding site must be highly complementary (i.e., lock and key) for efficient binding; the
antigen may induce a shape change of the antigen-binding site (induced fit mechanism); high
complementarity of epitope and binding site provides for the high specificity associated with
antigen-antibody binding
4. Opsonization—coating a bacterium with antibodies or complement to stimulate phagocytosis
Immunoglobulin classes
1. IgG—major Ig in human serum; monomeric protein; 80% of Ig pool
a. Antibacterial and antiviral
b. Enhances opsonization; neutralizes toxins
c. Only IgG is able to cross placenta (naturally acquired passive immunity for newborn)
d. Activates the complement system by the classical pathway
e. Four subclasses with some differences in function
2. IgM—pentameric protein joined with J chain at Fc ends; 8% of Ig pool
a. First antibody made during B-cell maturation and first antibody secreted during primary
antibody response
b. Never leaves the bloodstream
c. Agglutinates bacteria and activates complement by classical pathway; enhances
phagocytosis of target cells
d. Some may be red blood cell agglutinins
e. Up to 5% may be hexameric; hexameric form is better able to activate the complement
system than pentameric IgM; bacterial cell wall antigens may directly stimulate B cells to
produce hexameric form
3. IgA—12% of Ig pool
a. Some monomeric forms in serum, but most is dimeric (using a J chain) and associates
with a protein called the secretory component (secretory IgA or sIgA)
b. sIgA is primary Ig of mucosal-associated lymphoid tissue; also found in saliva, tears, and
breast milk (protects nursing newborns); helps rid the body of antigen-antibody
complexes by excretion; functions in alternate complement pathway
4. IgD—monomeric protein; trace amounts in serum
a. Does not activate the complement system and cannot cross the placenta
b. Abundant on surface of B cells where it plays a role in signaling B cells to start antibody
production
5. IgE—monomeric protein; a small percentage of Ig pool
a. Skin-sensitizing and anaphylactic antibodies
b. When an antigen cross-links two molecules of IgE on the surface of a mast cell or
basophil, it triggers release of histamine; stimulates eosinophilia and gut hypermotility,
which help to eliminate helminthic parasites
Antibody kinetics
1. Primary antibody response—when exposed to antigen (by infection or vaccination), levels
(titer) of antibody change over time
a. Initial lag phase of several days
b. Log phase—antibody titer rises logarithmically
c. Plateau phase—antibody titer stabilizes
d. Decline phase—antibody titer decreases because the antibodies are metabolized or
cleared from the circulation
e. IgM appears first, then IgG; relatively low antigen affinity
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Prescott’s Microbiology, 9th Edition
2.
Secondary antibody response (anamnestic response)—has shorter lag phase, higher antibody
titer, and more IgG, that have high affinity for antigens
F. Diversity of antibodies—several mechanisms contribute to the generation of antibody diversity
1. Combinatorial joining
a. Ig genes are interrupted or split genes with many exons; in light-chain gene, there are
three types of exons (C, V, and J); in heavy-chain gene, there are four types of exons (C,
V, J, and D)
b. During differentiation of B cells, one C exon, one V exon, and one J exon are joined
together to make a functional light-chain gene; one C, one V, one J, and one D are joined
together to make a functional heavy-chain gene; since there are numerous C, V, J, and D
exons, many different combinations are possible (2 x 10 8); different heavy chain
combinations can change the class of the antibody (antibody class switching)
2. Splice-site variability—the same exons can be joined at different nucleotides, thus generating
different codons and the possible diversity
3. Somatic mutations—the V regions of germ-line DNA are susceptible to a high rate of somatic
mutation during B-cell development
4. The number of different antibodies possible is the product of the number of light chains
possible and the number of heavy chains possible
G. Clonal selection
1. Because of combinatorial joining and somatic mutation, there are a small number of B cells
capable of responding to any given antigen; each group of cells is derived asexually from a
parent cell and is referred to as a clone; there is a large, diverse population of B-cell clones
that collectively are capable of responding to many possible antigens
2. Identical antibody molecules, specific to each B cell and a single antigen, are integrated into
the plasma membrane of B cell; when these bind the appropriate antigen, the B cell is
stimulated to divide and differentiate into two populations of cells: plasma cells and memory B
cells
a. Plasma cells are protein factories that produce about 2,000 antibodies per second for
their brief life span (5 to 7 days)
b. Memory B cells can initiate antibody-mediated immune response if they are stimulated
by being bound to the antigen; they circulate more actively from blood to lymph and have
long life spans (years or decades); are responsible for rapid secondary response; are not
produced unless B cell has been appropriately signaled by activated T-helper cell
3. Monoclonal antibodies – isolation of a single activated B plasma cell and fusion of it to a
transformed cell to generate a hybrid which yields a single type of antibody of high binding
specificity and affinity ; mAb drugs used to treat diseases such as autoimmune and some cancers.
VIII. Action of Antibodies
A. Neutralization
1. Adherence inhibition—sIgA prevents bacterial adherence to mucosal surfaces
2. Toxin neutralization—antibody (antitoxin) binding to toxin renders the toxin incapable of
attachment or entry into target cells
3. Viral neutralization—binding prevents virus from binding to and entering target cells
B. Opsonization—enhancement of phagocytosis; results from coating of microorganisms or other
material by antibodies or complement; forms bridge between the antigen and the phagocyte
C. Immune complex formation—two or more antigen-binding sites per antibody molecule lead to
cross-linking, forming molecular aggregates called immune complexes; these complexes are more
easily phagocytosed
1. Precipitation (precipitin) reaction—soluble particles are cross-linked, causing them to
precipitate from solution; the antibody involved is called a precipitin antibody
2. Agglutination reaction—particles or cells are cross-linked, forming an aggregate; the antibody
involved is called an agglutinin.
3. A variety of in vitro diagnostic assays rely on immune complex formation to detect the
presence of antigen or antibody
IX. Acquired Immune Tolerance
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Prescott’s Microbiology, 9th Edition
A.
X.
Nonresponse to self; three mechanisms have been proposed: negative selection by clonal deletion,
induction of anergy, and inhibition of immune response by T cells with suppressor/regulatory
function
1. Negative selection by clonal deletion—T cells with ability to interact with self-antigens are
destroyed in the thymus
2. Induction of anergy—an example of peripheral tolerance (tolerance that develops in areas
other than thymus); lymphocytes that can interact with self-antigens are given incomplete
activation signals, causing them to enter into an unresponsive state known as anergy
Immune Disorders
A. Hypersensitivities—exaggerated or inappropriate immune responses that result in tissue damage to
the individual; fall into four types following the Gell-Coombs classification system
1. Type I hypersensitivity—includes allergic reactions
a. Occurs immediately following second contact with responsible antigen (allergen); on first
exposure, B cells form plasma cells that produce IgE (reagin), which binds to mast cells
or basophils via Fc receptors and sensitizes them; upon subsequent exposure, the allergen
binds to these IgE-bearing cells; physiological mediators released by this binding cause
anaphylaxis (smooth muscle contraction, vasodilation, increased vascular permeability,
and mucus secretion)
b. Systemic anaphylaxis results from a massive release of these mediators, which cause
respiratory impairment, lowered blood pressure, and serious circulatory shock; death can
occur within a few minutes
c. Localized anaphylaxis (atopic reaction) includes hay fever in the upper respiratory tract
d. Skin testing is used to identify allergens; small amounts of possible allergens are
inoculated into skin; rapid inflammatory reaction indicates sensitivity
e. Desensitization to allergens involves controlled exposure to the allergen in order to
stimulate IgG production; IgG molecules serve as blocking antibodies that intercept and
neutralize the allergen before it can bind to the IgE-bound mast cells
2. Type II hypersensitivity—generally cytolytic or cytotoxic reaction that destroys host cells
a. IgG or IgM antibodies are directed against cell surface or tissue antigens; this stimulates
complement pathway and a variety of immune effector cells
b. Blood types (ABO blood groups) are determined by cell surface glycoproteins on red
blood cells; types A, B, and AB have specific cell surface proteins while type O has
none; ABO glycoproteins are self antigens; there is an intense immune response to
transfusions of blood that does not match the host type
c. Rh factor is another blood antigen that is either present or absent in an individual;
incompatibility between Rh- mothers and Rh+ fetuses can induce anti-Rh antibodies that
destroy fetal blood cells in a syndrome called erythroblastosis fetalis
3. Type III hypersensitivity
a. Involves formation of immune complexes, which in the presence of excess antigen are
not efficiently removed; their accumulation triggers complement-mediated inflammation
b. Can cause inflammation and damage to blood vessels (vasculitis), kidney glomerular
basement membranes (glomerulonephritis), joints (arthritis), and skin (systemic lupus
erythematosus)
4. Type IV hypersensitivity—involves TH1 lymphocytes or CTLs that migrate to and accumulate
near the antigen; this is a time-delayed response
a. Presentation of antigen to TH1 or CTL cells causes the release of cytokines; these attract
macrophages and basophils to the area, leading to inflammatory reactions that can cause
extensive tissue damage
b. Can be used diagnostically, as in the tuberculin skin test (for tuberculosis exposure)
c. Examples of type IV hypersensitivities include allergic contact dermatitis (poison ivy,
cosmetic allergies) and some chronic diseases (leprosy, tuberculosis, leishmaniasis,
candidiasis, herpes simplex lesions)
B. Autoimmunity and Autoimmune diseases
1. Autoimmunity is characterized by the presence of autoantibodies; autoimmune disease results
from activation of self-reactive T and B cells, which leads to tissue damage
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Prescott’s Microbiology, 9th Edition
2.
C.
D.
More common in older individuals; may involve viral or bacterial infections that cause tissue
damage and the release of abnormally large quantities of antigen, or that cause some selfproteins to alter their form so that they are no longer recognized as self
Transplantation (tissue) rejection
1. Transplantation of tissue from one individual to another can be an allograft (donor and
recipient are genetically different individuals of the same species) or xenograft (donor and
recipient are different species)
2. Mechanisms of tissue rejection
a. Foreign class II MHC antigens trigger T H cells to help CTL cells destroy the graft; the
CTL cells recognize the graft as foreign by detecting the class I MHC antigens of the
graft
b. TH cells may react directly with the graft, releasing cytokines that stimulate macrophages
to enter the graft and destroy it
3. Graft-versus-host reaction—immunocompetent cells in donor tissue (e.g., bone marrow) reject
the immunosuppressed host
Immunodeficiencies—failure to recognize and/or respond properly to antigens
1. Primary (congenital) immunodeficiencies result from a genetic disorder (usually on X
chromosome)
2. Secondary (acquired) immunodeficiencies result from infection by immunosuppressive
microorganisms (e.g., AIDS, chronic mucocutaneous candidiasis) or immunosuppressive
drugs.
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Prescott’s Microbiology, 9th Edition
CRITICAL THINKING
1.
Draw the basic structure of all immunoglobulin molecules and label the following: Fc, Fab, constant
regions, variable regions, antigen-binding sites, heavy chains, and light chains. Correlate the constant and
variable regions of each chain to their coding regions in the germline DNA.
2.
Macrophages and other phagocytic cells have relatively nonspecific targets. Explain how cytokines
increase the apparent specificity of these effector cells. In your discussion indicate why this is an
apparent and not an actual change in specificity, even though the result is indeed a more specific
destruction of the invading organism.
3.
CD4+ cells are among the primary targets of human immunodeficiency virus (HIV). As HIV infection
progresses, the number of CD4+ cells declines, causing a weakening of both the cellular and humoral
immune responses. Explain why the targeting of this single type of lymphocyte has such broad impact on
the functioning of the immune system.
4.
Why is it prudent that two signals are required for B and T cell activation , but only one signal is required
for an antigen presenting cell (APC)?
CONCEPT MAPPING CHALLENGE
Use the following words to construct a concept map by providing your own linking words:
Cellular immunity Humoral immunity T cells B cells Acquired immunity Memory
Specificity Cytotoxic T cells T-helper cells Plasma cells MHC proteins
Vaccines
Presenting Cells
Memory T cells Memory B cells
Antibodies
Antigen
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