6-12

Objective 6 – Immunity Overview

Two Intrinsic Defense Systems

Non-Specific (Innate)

  • Immediate response; pre-formed.

  • Broad range of targets.

  • Structures:

    • Barriers (skin, mucous membranes).

    • Chemicals.

    • Cells (phagocytes, NK cells).

Specific (Adaptive)

  • Delayed response.

  • Very selective.

  • Cells:

    • B lymphocytes, T lymphocytes, macrophages.

Objective 7 – Non-Specific Resistance

1. Barriers

Skin

  • 30–50 layers of stratified keratinized epithelium.

  • Acidic pH (3–5).

  • Salty (NaCl in sweat).

  • Dry.

  • Secretions: lysozyme, fatty acids.

  • Normal flora compete with pathogens.

Mucous Membranes

  • Non-keratinized stratified squamous epithelium.

  • Acidic in stomach & vagina.

  • Hair, cilia, mucous trap particles.

  • Saliva contains lysozyme.

  • Normal flora in respiratory & digestive tracts.

2. Cells

Phagocytes

  • Macrophages, neutrophils, eosinophils (weak), mast cells.

  • Use free radicals (NO), H₂O₂, defensins.

NK Cells

  • Large granular lymphocytes.

  • Release perforins + granzyme B → apoptosis of virus-infected or cancer cells.

3. Antimicrobial Proteins

Interferon (α, β, γ)

  • Antiviral effects: stimulates PKR to block viral protein synthesis.

  • Activates macrophages + NK cells.

Complement

  • 20 plasma proteins (C1–C9 + factors B, D, properdin).

  • Functions:

    1. Amplify inflammation.

    2. Cause pathogen lysis.

  • Pathways

    1. Classical: requires antibody–antigen complexes.

    2. Alternative: microbial polysaccharides.

    3. Lectin: lectin + microbial sugars.

  • C3a → inflammation

  • C3b → opsonization

  • C5–C9 → MAC → cell lysis.

C-Reactive Protein

  • Liver-made acute phase protein.

  • Binds pathogens/damaged cells → activates classical complement.

4. Inflammation

  • Nonspecific vascular response.

  • Goals: destroy agents, wall off area, enhance immune response, promote healing.

Vascular Changes

  • Vasodilation → redness, heat, more O₂/nutrients/WBCs.

  • Increased permeability → fluid + proteins → edema → pain.

Phagocyte Mobilization

  1. Leukocytosis

  2. Margination

  3. Diapedesis

  4. Chemotaxis

Cardinal Signs

  • Swelling, redness, heat, pain.

Objective 8 – Characteristics of Immune Responses

Every immune response:

  1. Antigen-specific

  2. Systemic

  3. Has memory

Objective 9 – Humoral vs. Cell-Mediated Immunity

Humoral Immunity (B cells)

  • Plasma cells secrete antibodies into body fluids.

  • Antibodies bind antigens →

    • Activate complement

    • Neutralize

    • Precipitate

    • Agglutinate

Definitions

  • Neutralization: antibody blocks antigen’s active site.

  • Agglutination: cross-linking of large antigens → clumping.

  • Precipitation: soluble antigens form insoluble complexes.

Cell-Mediated Immunity (T cells)

  • T cells travel to infection site.

  • Act directly (lysis) or indirectly (activate other immune cells).

Objective 10 – Cells of the Adaptive Immune System

1. Antigen-Presenting Cells (APCs)

  • Dendritic cells, macrophages, B cells.

  • Engulf antigens → present fragments to T/B cells.

MHC Molecules

  • Class I

    • Location: all nucleated cells.

    • Recognized by CD8.

  • Class II

    • Location: dendritic cells, macrophages, B cells.

    • Recognized by CD4.

2. B Lymphocytes

  • Mature in bone marrow.

  • Acquire surface antibody (BCR).

  • Self-reactive ones are deleted or inactivated.

  • Activation →

    • Plasma cells (secrete antibodies)

    • Memory cells

3. T Lymphocytes

  • Mature in thymus; acquire TCR.

  • Must pass:

    • Positive selection (bind MHC I).

    • Negative selection (must not bind self antigens).

T Cell Subsets

  • Helper T (CD4)

    • Activated by APC + MHC II.

    • TH1: inflammation, macrophage activation, cytotoxic T activation.

    • TH2: eosinophil recruitment, B-cell activation.

  • Cytotoxic T (CD8)

    • Directly attack infected, cancerous, or transplanted cells.

    • Release cytokines, induce apoptosis.

  • Regulatory T (CD4)

    • Release IL-10, TGF-β, γ-interferon to suppress immune response.

Objective 11 – Antigens

Definitions

  • Antigens (immunogens) = substances that evoke immune responses.

  • Characteristics:

    1. Large

    2. Complex

    3. Non-self

Complete Antigens

  • Have immunogenicity (activate B/T cells)

  • Have reactivity (react with antibodies/T cells)

Incomplete Antigens (Haptens)

  • Too small alone → become antigenic when attached to carrier proteins.

Antigenic Determinants (Epitopes)

  • Actual portions of antigen that are immunogenic.

Objective 12 – Humoral Response to Antigen (Based on Images)

I. Primary Response (first exposure to antigen)

1. Antigen recognition

  • A B lymphocyte encounters an antigen.

  • Only the B cell with a complementary receptor binds the antigen.

  • Non-matching B cells remain inactive.

2. B-cell activation

  • After binding antigen, the B cell waits for activation by a Helper T cell.

  • Helper T cell interaction confirms the threat (“permission to activate”).

3. Clonal selection & proliferation

  • The activated B cell becomes a B lymphoblast.

  • It undergoes rapid mitosis to form a clone of identical B cells.

  • The clone differentiates into:

    • Plasma cells

    • Memory B cells

4. Plasma cell function

  • Plasma cells secrete large quantities of antibodies specific to the antigen.

  • Antibodies attach to the invader, marking it for destruction.

5. Effector actions on pathogen

  • Antibody-tagged pathogens are targeted by “eater cells” (phagocytes).

  • Phagocytes prefer invaders coated in antibodies (“This one looks delicious!”).

II. Secondary Response (subsequent exposure to same antigen)

1. Memory B cells respond

  • Memory B cells created during the primary response remain in the body.

  • Upon a second exposure:

    • They quickly recognize the antigen (“I remember this one!”).

    • They activate much faster than naïve B cells.

2. Rapid plasma cell formation

  • Memory cells immediately divide into large numbers of plasma cells.

  • Plasma cells again release antibodies—but much more quickly and in higher amounts.

3. Stronger, faster immunity

  • The secondary response:

    • Produces more antibodies

    • Responds faster

    • Provides long-term protection

III. Overall Flow (Combined from Both Images)

  1. B cell finds matching antigen

  2. Helper T cell activates the B cell

  3. Clonal expansion → plasma cells + memory cells

  4. Plasma cells produce antibodies

  5. Antibodies tag pathogens → phagocytes destroy them

  6. Memory cells stay for future exposures

  7. Secondary exposure → rapid, intense antibody production