Topic 25- Adaptive Immunity

I. Introduction to Adaptive Immunity

A. What Is Adaptive Immunity?

Adaptive immunity is the body's targeted defense system that develops after exposure to specific pathogens. It contrasts with innate immunity, which is present from birth and responds non-specifically.

• Active Immunity: Your own immune system produces antibodies and memory cells.

• Passive Immunity: Borrowed immunity (e.g., from mother via placenta or antibody injections).

• Natural Immunity: Acquired through natural exposure to pathogens.

• Artificial Immunity: Induced by vaccines or booster shots.

• Development Time: Adaptive immunity typically takes about 28 days to fully develop a robust memory response.

B. Lymphocytes: The Key Players

C. Key Terms

• Antigen: A foreign substance that triggers an immune response (usually proteins or polysaccharides).

• Epitope: The specific site on an antigen recognized by B or T cell receptors.

• Antibody (Immunoglobulin/Ig): A protein produced by B cells to bind antigens and neutralize or mark pathogens.

D. Major Features of Adaptive Immunity

1. Diversity:

   • 1 million B-cell receptor types

   • 10 million T-cell receptor types

   • Enables recognition of vast array of pathogens.

2. Self-Tolerance:

   • Prevents attack on own body.

3. Immunological Memory:

   • Primary Response: Slower (10–17 days), first exposure.

   • Secondary Response: Faster (2–7 days), upon re-exposure.

4. Clonal Expansion:

   • Activation causes B/T cells to divide:

     • Effector cells: Active fighters.

     • Memory cells: Long-lived cells for faster future response.

II. B Cells and T Cells

A. B Cells (Humoral Immunity)

• Receptors shaped like a “Y” that bind directly to antigens.

• Do not need infected cells to display antigens.

• B cells:

  1. Wait until encountering a matching antigen.

  2. Bind to it and become activated.

  3. Proliferate and produce antibodies.

  4. Antibodies help neutralize pathogens in blood and lymph.

B. T Cells (Cell-Mediated Immunity)

• Receptors not Y-shaped; bind only to antigen fragments presented by other cells.

• Types:

  1. Helper T-cells (CD4+): Activate B cells and cytotoxic T-cells.

  2. Cytotoxic T-cells (CD8+): Kill infected cells directly.

• Require antigen-presenting cells (APCs) or infected cells to show antigen fragments via MHC molecules.

III. Immune Response to Antigen

A. Helper T-Cells: The Coordinators

1. Detect antigens on APCs.

2. Release cytokines that:

   • Stimulate cytotoxic T-cells (cell-mediated response).

   • Stimulate B-cells (humoral response).

B. Cytotoxic T-Cells: The Assassins

• Kill infected cells using:

  • Perforin: Creates pores in infected cell membranes.

  • Granzymes: Trigger apoptosis (cell death).

• Require activation signals from helper T-cells.

C. B Cells and Antibody Production

• Upon activation:

  1. Multiply and differentiate into plasma cells.

  2. Secrete antibodies that:

     • Neutralize pathogens.

     • Tag them for destruction by other immune cells.

D. Complement System: Antibody Assistants

• A protein cascade that:

  1. Neutralizes viruses by preventing cell entry.

  2. Opsonizes bacteria to enhance phagocytosis.

  3. Forms pores in foreign cells, causing lysis (bursting).

IV. Vaccines

A. How Vaccines Work

• Introduce a harmless form of a pathogen to the body.

• Stimulates the adaptive immune system without causing disease.

• Leads to immunological memory and rapid future responses.

B. Types of Vaccines

C. Challenges in Vaccine Design

• Antigenic drift: Small mutations → new strains each year (e.g., flu).

• Antigenic shift: Large recombination events → pandemics.

• Strain replacement: Less common strain becomes dominant after vaccination suppresses the more common one.

D. Herd Immunity

• If a critical mass is immune, the disease cannot spread easily.

• Measured by R₀ (basic reproduction number):

  • If R₀ = 4, each person could infect 4 others.

  • Vaccinating enough people lowers spread even for the unvaccinated.