Adaptive Immunity — B and T Cell Function, Antibody Diversity, and MHC Explained | Chapter 27 from Brock Biology of Microorganisms

How does your immune system generate targeted, lasting defense against countless threats? Chapter 27 of Brock Biology of Microorganisms unpacks the complexity of adaptive immunity—the body’s highly specific, memory-forming response to infection. This summary explores B and T lymphocyte development, antibody diversity, the critical role of MHC molecules, and how these elements coordinate to maintain health and prevent autoimmunity.

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Key Properties of Adaptive Immunity: Specificity, Memory, and Tolerance

Adaptive immunity is characterized by:

• Specificity: B cell (BCR) and T cell (TCR) receptors recognize unique antigens with high precision.
• Memory: After a primary infection, memory cells ensure a faster and stronger response to subsequent exposures.
• Tolerance: Mechanisms eliminate or suppress self-reactive lymphocytes, preventing autoimmune disease.

Lymphocyte Development and Selection

All adaptive immune cells arise from hematopoietic stem cells:

• T cells mature in the thymus, undergoing:
  • Positive selection: Survival of cells that recognize self-MHC.
  • Negative selection: Elimination of cells with strong self-reactivity.
• B cells mature in bone marrow; self-reactive B cells are removed by apoptosis or become anergic (unresponsive).

Antigens, Immunogens, and Immunity Types

• Antigens: Any molecule recognized by immune receptors.
• Immunogens: Antigens that actually elicit an immune response.
• Epitopes: Specific antigenic sites recognized by antibodies or TCRs.
• Active immunity: Develops after exposure or vaccination.
• Passive immunity: Antibodies transferred from another source (e.g., mother to child).

B Cell Activation and Antibody Classes

When a B cell’s receptor (BCR) binds an antigen and receives help from a T-helper cell, it proliferates into plasma cells (antibody factories) and memory cells.

• T-independent antigens can activate B cells without T cell help, but elicit weaker responses.
• Antibody structure: Y-shaped; two heavy and two light chains, with Fab (antigen-binding) and Fc (effector function) regions.
• Isotypes:
  • IgG: Most abundant; crosses placenta.
  • IgM: First antibody produced; strong complement activator.
  • IgA: Secreted at mucosal surfaces.
  • IgD: B cell receptor (function less clear).
  • IgE: Allergies and parasite defense.

Primary vs. Secondary Response

The primary immune response is slow and mostly produces IgM. Memory cell formation leads to a rapid, robust, mostly IgG response on subsequent exposures—a principle that underpins vaccination.

Antibody and TCR Diversity Mechanisms

Adaptive immunity’s remarkable diversity comes from:

• Somatic recombination of V(D)J gene segments.
• Junctional diversity via imprecise joining.
• N and P nucleotide additions during gene rearrangement.
• Allelic exclusion ensures one unique receptor per lymphocyte clone.
• Somatic hypermutation and affinity maturation (in B cells) improve binding after antigen exposure.
• TCRs also rely on gene rearrangement for diversity, but do not undergo hypermutation.

MHC and Antigen Presentation

Major Histocompatibility Complex (MHC) molecules are essential for T cell recognition:

• MHC I: Present on all nucleated cells; present endogenous antigens to CD8+ cytotoxic T (Tc) cells.
• MHC II: Found on antigen-presenting cells (APCs); present exogenous antigens to CD4+ helper T (Th) cells.
• Antigen loading:
  • MHC I: Loaded in the endoplasmic reticulum via TAP proteins.
  • MHC II: Loaded in lysosomes after invariant chain removal.
• MHC is highly polymorphic and polygenic, ensuring recognition of a broad range of antigens. MHC mismatches can cause transplant rejection.

T Cell Activation and Subsets

T cell activation requires two signals: TCR-peptide-MHC binding and costimulation (e.g., CD28-B7 interaction). Without both signals, T cells become anergic (non-responsive).

• T cell subsets:
  • Cytotoxic T (Tc, CD8+): Kill infected cells via perforin and granzymes.
  • Helper T (Th, CD4+): Coordinate immune responses.
    • Th1: Activate macrophages, support cell-mediated immunity.
    • Th2: Stimulate B cells for antibody production.
    • Th17: Recruit neutrophils (via IL-17).
    • Treg: Suppress autoimmunity (via IL-10, TGF-β).

Glossary: Key Terms from Chapter 27

• CDR: Complementarity-determining region (antigen-binding site).
• Clonal selection: Expansion of antigen-specific lymphocytes.
• MHC: Major histocompatibility complex for antigen presentation.
• TCR: T cell receptor recognizing peptide–MHC.
• Tolerance: Unresponsiveness to self-antigens.
• Affinity maturation: Selection for stronger antigen binders.
• Memory cells: Long-lived defenders for future exposures.
• Immunogen vs. antigen: Immunogens elicit responses; antigens bind immune receptors.

Conclusion: Adaptive Immunity and the Future of Medicine

Chapter 27 highlights how B and T lymphocytes, clonal selection, MHC molecules, and antibody diversity equip the body for lifelong protection. These principles underpin modern immunology, vaccine development, and therapies for infection, cancer, and autoimmunity.

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