(Chapter 17, Part 1) Adaptive Immunity: Specific Defenses of the Host

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Adaptive Immunity: Specific Defenses of the Host

Introduction to Adaptive Immunity

Adaptive immunity is a highly specialized defense system that targets specific pathogens after exposure. It distinguishes 'self' from 'nonself' and is activated when innate defenses fail to stop a microbe. Adaptive immunity is acquired through infection or vaccination and involves two main responses:

Primary response: The first time the immune system combats a particular foreign substance.
Secondary response: Subsequent interactions with the same foreign substance; faster and more effective due to 'memory'.

The Dual Nature of the Adaptive Immune System

Humoral Immunity

Humoral immunity involves the production of antibodies that combat foreign molecules known as antigens. B cells are lymphocytes created and matured in red bone marrow, and they recognize antigens and make antibodies. In birds, B cells are named after the bursa of Fabricius, but in humans, they reside in the blood and lymphoid organs.

Cellular Immunity (Cell-Mediated Immunity)

Cellular immunity involves T lymphocytes, which recognize antigenic peptides processed by phagocytic cells. T cells mature in the thymus and reside in blood and lymphoid organs. T cell receptors (TCRs) on the T cell surface contact antigens, causing the T cells to secrete cytokines instead of antibodies. Cellular immunity is best at fighting virus-infected cells and intracellular bacteria.

Comparison of Humoral and Cellular Immunity

Cellular immunity attacks antigens that have already entered cells (e.g., viruses, some intracellular bacteria such as M. leprae and L. monocytogenes).
Humoral immunity fights invaders and threats outside cells (e.g., extracellular bacteria and toxins, viruses before they enter a host cell).

Cytokines: Chemical Messengers of Immune Cells

Cytokines are protein messengers produced in response to a stimulus. They include:

Interleukins (ILs): Communicate between leukocytes.
Chemokines: Induce migration of leukocytes.
Interferons (IFNs): Interfere with viral infections of host cells.
Tumor necrosis factor alpha (TNF-α): Involved in inflammation of autoimmune diseases.
Hematopoietic cytokines: Control stem cells that develop into red and white blood cells.

Overproduction of cytokines leads to a cytokine storm.

Key Cytokines and Their Roles

Type	Source	Target Cells	Function
IL-1	Macrophages	Helper T cells	Stimulates helper T cells
IL-2	Helper T cells	Helper T cells, cytotoxic T cells, NK cells	Stimulates proliferation
IL-4	Helper T cells	B cells	Promotes antibody production
IL-17	Helper T cells	Neutrophils	Promotes inflammation
IFN-γ	T cells, NK cells	Macrophages	Activates macrophages
TNF-α	Macrophages	Various cells	Promotes inflammation
Additional info:	Other cytokines exist with specialized functions.

Table 17-1 Key Cytokines and Their Roles

Antigens and Their Properties

Antigens are substances that cause the production of antibodies. They are usually components of invading microbes or foreign substances, such as cell walls, flagella, fimbriae, toxins, capsules, and viral spikes. Nonmicrobial antigens may include egg white, pollen, and cell surface molecules.

Antibodies interact with specific regions (epitopes or antigenic determinants) on the antigen.
Haptens are molecules too small to be antigenic; they attach to carrier molecules and provoke an immune response.

Figure 17-2 Epitopes (Antigenic Determinants) Figure 17-3 Haptens

Humoral Immunity: Antibodies

Antibodies, also known as immunoglobulins (Ig), are compact soluble proteins that recognize and bind to specific antigens, targeting them for destruction. The valence is the number of antigen-binding sites on an antibody; bivalent antibodies have two binding sites.

Four protein chains form a Y shape: two identical light chains and two identical heavy chains joined by disulfide links.
Variable (V) regions are at the ends of the arms and bind epitopes.
Constant (C) region is the stem, which is identical for a particular Ig class.
Five classes of Ig: IgG, IgM, IgA, IgD, IgE.

Figure 17-4 Structure of a Typical Antibody

Immunoglobulin Classes

Class	Structure	Serum %	Location	Function
IgG	Monomer	80%	Blood, lymph, intestine	Crosses placenta, protects fetus, activates complement, enhances phagocytosis, neutralizes toxins/viruses
IgM	Pentamer	6%	Blood vessels	First response, agglutination, activates complement
IgA	Monomer/dimer	13%	Mucous membranes, secretions	Prevents microbial attachment
IgD	Monomer	0.02%	Blood, lymph, B cells	Membrane immunoglobulin on B cells
IgE	Monomer	0.002%	Mast cells, basophils, blood	Histamine release, parasitic worms, allergies

Table 17-2 A Summary of Immunoglobulin Classes

Humoral Immunity Response Process

B cells reside in and interact with antigens in lymphoid organs (spleen and lymph nodes). Each B cell has over 100,000 membrane-bound surface immunoglobulins that serve as antigen receptors. The process involves:

Clonal selection: B cell is activated when its B-cell receptor (BCR) binds to its antigen.
Clonal expansion: The activated B cell proliferates and differentiates into plasma cells (secrete antibody) and memory B cells.

Activation and Clonal Expansion of Antibody-Producing Cells

T-Dependent and T-Independent Antigens

T-dependent antigens: Require a T helper cell (Th) for activation; include proteins from viruses, bacteria, red blood cells.
T-independent antigens: Do not need Th assistance; often polysaccharides from bacterial capsules or LPS.

Figure 17-5 Activation of B Cells Against a T-Dependent Antigen Figure 17-6 Clonal Selection and Differentiation of B Cells Figure 17-7 Activation of B Cells Against a T-Independent Antigen

Major Histocompatibility Complex (MHC)

Antigen-presenting cells must display antigen on their surface in association with MHC class II molecules.
MHC genes encode molecules on the cell surface.
Class I MHC: On the membrane of nucleated cells; identifies cell as 'self'.
Class II MHC: On the surface of antigen-presenting cells (APCs), including B cells, macrophages, dendritic cells.

Activation Process

Inactive B cells contain surface Ig that bind to antigen.
B cell internalizes and processes antigen; antigen fragments are displayed on MHC Class II molecules on B cell surface.
T helper cell (Th) contacts the displayed antigen fragment and releases cytokines that activate B cells.
B cell undergoes proliferation (clonal expansion) and differentiation, producing antibody-producing plasma cells and memory cells.

The Diversity of Antibodies

The estimated extent of antibody diversity is 1011 (100 billion) different antibodies. Immunoglobulin genes have segments that can rearrange to produce diversity in the antigen-binding section of the antibody molecule. Clonal deletion removes potentially harmful self-reactive B cells.

Results of the Antigen-Antibody Interaction

An antigen-antibody complex forms when antibodies bind to antigens. The strength of the bond is the affinity. Antibodies protect the host by tagging foreign molecules or cells for destruction. The main results include:

Agglutination
Opsonization
Antibody-dependent cell-mediated cytotoxicity
Neutralization
Activation of the complement system

Figure 17-8 The Results of Antigen-Antibody Binding

Cellular Immunity Response Process

T cells combat intracellular pathogens and abnormal host cells such as cancer cells. They mature in the thymus, and thymic selection eliminates immature and self-reactive T cells. T cells migrate from the thymus to lymphoid tissues and attach to antigens via T-cell receptors (TCRs).

Lymphocyte (Red) Attaches to Cancer Cell (Blue)

Pathogen Entry and M Cells

Pathogens entering the gastrointestinal tract pass through microfold cells (M cells) located over Peyer's patches (aggregated lymphoid nodules). These cells transfer antigens to lymphocytes and antigen-presenting cells (APCs).

Figure 17-9 M Cells

Summary Table: Immunoglobulin Classes

Class	Structure	Serum %	Location	Function
IgG	Monomer	80%	Blood, lymph, intestine	Crosses placenta, protects fetus, activates complement, enhances phagocytosis, neutralizes toxins/viruses
IgM	Pentamer	6%	Blood vessels	First response, agglutination, activates complement
IgA	Monomer/dimer	13%	Mucous membranes, secretions	Prevents microbial attachment
IgD	Monomer	0.02%	Blood, lymph, B cells	Membrane immunoglobulin on B cells
IgE	Monomer	0.002%	Mast cells, basophils, blood	Histamine release, parasitic worms, allergies

Additional info:

Adaptive immunity is a cornerstone of vaccine development and immunotherapy.
Memory cells are critical for long-term protection against pathogens.
Immunoglobulin diversity is generated by gene rearrangement and somatic hypermutation.