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Adaptive Immunity: T Cells, B Cells, Antibodies & Inflammation

Major Histocompatibility Complex (MHC) and T-Cell Activation

  • Two structurally and functionally distinct classes of MHC molecules mediate antigen presentation.

    • MHC Class I

    • Expressed on all nucleated cells of the body.

    • Presents endogenous (intracellular) peptide fragments to \text{CD8}^+ cytotoxic T lymphocytes (CTLs).

    • MHC Class II

    • Restricted to professional antigen-presenting cells (APCs): dendritic cells, macrophages, B cells (and specialized epithelial cells).

    • Presents exogenous (extracellular) peptides to \text{CD4}^+ helper T cells (Th cells).

  • Key examination cue: “Which class of MHC is found only on APCs?” → MHC II.

Activation Signals for T Cells

  1. Helper T‐cell (CD4+) activation

    • Requires an APC displaying antigen via MHC II.

    • Secondary co-stimulatory interactions (e.g.
      \text{CD28}–\text{B7}) stabilize and finalize activation.

  2. Cytotoxic T‐cell (CD8+) activation

    • Signal 1: Recognition of an infected/self cell displaying antigen via MHC I → “learning.”

    • Signal 2: Co-stimulation from helper T cells and APC cytokines → “license to kill.”

Fate of Activated T Lymphocytes

  • Proliferation: rapid mitotic expansion (clone size increases).

  • Differentiation: daughter cells adopt two major phenotypes.

    • Effector cells

    • Immediate actors; execute killing (CD8+) or coordinate immune responses (CD4+).

    • Memory cells

    • Long-lived sentinels; provide faster, stronger response upon re-exposure.

  • Clinical relevance: Booster vaccines raise the number of both effector and memory clones when titers wane.

Mechanisms of Cytotoxicity (Slide 94 Focus)

  • Cytotoxic T lymphocytes (CTLs / CD8+) kill virus-infected or altered self cells via granule exocytosis.

    1. Perforin

    • Polymerizes to form transmembrane pores → “perforates” target membrane → increases permeability.

    1. Granzymes

    • Serine proteases that enter through perforin pores → initiate caspase cascade → apoptosis (controlled cell shrinkage, not lysis).

  • Parallel system: Natural killer (NK) cells employ the same perforin–granzyme axis.

  • Because it operates on whole cells, this arm is termed cell-mediated immunity.

B Lymphocytes and Humoral Immunity

  • Origin & lifespan

    • Mature in bone marrow (no thymic phase).

    • Activated plasma cells survive ≈ 5 days, so the bone marrow continually produces new B cells.

  • Activated B-cell outcomes

    1. Plasma cells → secrete antibodies.

    2. Memory B cells → durable humoral memory (basis of serologic titers).

Antibody Titer (clinical laboratory term)

  • "Titer" = circulating blood concentration of antibodies against a specific antigen.

  • Used to verify vaccine status or past infection.

Antibody Effector Functions (NAP mnemonic)

  • Neutralization (large/toxic particles)

    • Antibody binds pathogen or toxin surface → blocks biological activity ("neutralizes").

  • Agglutination (cells/large particles)

    • Cross-linking of multivalent antigens → clumping of foreign cells, e.g.
      incompatible blood transfusion reactions.

  • Precipitation (soluble, small antigens)

    • Antibodies aggregate tiny antigens → form larger complexes that become visible & phagocytosable.

  • Opsonization (additional key term)

    • Antibody \text{Fc} region “tags” pathogen → enhances phagocyte recognition & uptake.

Primary vs. Secondary Humoral Responses

  • First exposure (primary)

    • Lag, then modest rise in \text{IgM} followed by \text{IgG}.

  • Second exposure (secondary / anamnestic)

    • Rapid, larger surge of \text{IgG}; smaller, brief \text{IgM} bump.

    • Exam pearl: “Which is higher in the secondary response?” → \text{IgG}.

Active vs. Passive Immunity

  • Active immunity

    • Immune system actively generates response.

    • Natural infection (common cold).

    • Vaccination (injected antigens or attenuated pathogens).

  • Passive immunity

    • Pre-formed antibodies are transferred.

    • Maternal transplacental IgG or breast-milk IgA (infant protection).

    • Antisera/antitoxins (e.g.
      anti-snake-venom IgG).

    • Duration: days to weeks (≤ ≈ 2 months); antibodies decay by apoptosis/degradation.

Effectors in Immunology vs. Neurobiology Analogy

  • Nervous system: efferent neurons → muscles & glands (effectors).

  • Immune system: antibodies & immune cells themselves are the effectors that execute the response.

Cardinal Signs of Inflammation (Slide reference)

  • Latin medical triad/quadrad:

    1. Rubor – redness.

    2. Calor – heat.

    3. Tumor – swelling.

    4. Dolor – pain.

  • (Some texts add Functio laesa – loss of function.)

Quick Terminology & Reminders

  • Proliferate = increase in cell number (mitosis).

  • Differentiate = diverge into distinct functional subsets.

  • Apoptosis = programmed cell death; cell shrinks, membrane integrity intact.

  • Perforin = pore-forming molecule; “perforates.”

  • Granzyme = serine protease; triggers apoptosis within target.

  • Effector (immune) = molecule or cell producing the defensive effect (antibodies, active CTLs, etc.).

  • \text{CD4}^+ (helper) ↔ \text{MHC II}; \text{CD8}^+ (cytotoxic) ↔ \text{MHC I}.

  • NAP mnemonic → sequence of picture labels: Neutralization – Agglutination – Precipitation.

These notes consolidate all major and minor teaching points, definitions, examples, and numerical facts mentioned in the transcript, forming a complete study roadmap for the upcoming quiz or exam.