LL2

Innate Defenses and Adaptive Immunity

Complement Proteins (C Proteins)

• Definition: Complement proteins, also known as C-reactive proteins, are a group of proteins that facilitate a domino effect leading to enhanced immune responses, particularly aiding antibodies in protection against pathogens.

Activation and Functions

• When complement proteins are activated, they cause:

  • Release of Histamine:

  • Histamine is released from mast cells and basophils (with mast cells localized in tissues and basophils in blood).

  • Effect: Increases blood flow and inflammatory response at sites of infection or damage.

  • Mechanism:

    • Histamine dilates blood vessels, enhancing nutrient and oxygen supply to the affected area.

    • Immune cells arrive at the infection site more quickly, limiting pathogen spread temporarily.

  • Chemotaxis: Attracts neutrophils and macrophages to the site of infection.

  • Enhancement of Phagocytosis:

  • Complement proteins coat microbial cells, providing more binding sites for phagocytic cells to latch onto, thereby facilitating phagocytosis.

  • Importance: For effective phagocytosis, the phagocyte must securely attach to the target cell being destroyed.

  • Membrane Attack Complexes (MAC):

  • Accomplished by the proteins creating structures that drill holes into the target cell's plasma membrane using perforins, leading to the target's destruction.

Summary Mechanisms of Action

1. Killing Pathogens: Perforins create holes in target cells, causing it to disintegrate.

2. Enhancing Phagocytosis: Coating of target cells provides additional anchoring points for phagocytosis.

3. Inducing Inflammation: Promotes blood flow to the site, facilitating immune response and nutrient delivery.

Inflammation

• Definition: A localized tissue response to injury, generally operating without autoimmune interference.

Cardinal Symptoms of Inflammation

1. Swelling (Tumor): Volume increase in affected tissue.

2. Redness (Rubor): Dilated blood vessels and increased blood flow.

3. Heat (Calor): Increased temperature due to enhanced blood flow.

4. Pain (Dolor): Sensation linked to the inflammatory response.

Effects of Inflammation

• Temporary Tissue Repair: Aids in local repair processes and restricts pathogen entry into the wound.

• Slows Pathogen Spread: Localized action to control and limit infection.

• Mobilization of Defenses: Increased circulation allows for swift deployment of immune cells to the injury.

• Tissue Repair: After injury, processes culminate in the removal of pathogens and cleanup of cell debris, leading to tissue repair and healing.

• Necrosis: Refers to tissue death that results in pus formation from cellular debris, fluids, and dead cells. Accumulation within closed spaces is termed an abscess.

Process of Inflammation

1. Tissue Damage: An injury induces mechanical or chemical changes in tissue fluid.

2. Mast Cell Activation: Damaged tissue activates mast cells, which release histamine and heparin.

   • Histamine: Causes blood vessel dilation and increases blood flow.

   • Heparin: Prevents blood clot formation, allowing fluid to leak and minimizing pathogen spread.

3. Phagocyte Mobilization: Neutrophils arrive, releasing cytokines that attract more immune cells.

4. Repair Process: Cytokines promote tissue repair, leading to clot erosion and scar formation.

Role of Fever

• Definition: Fever is characterized by a body temperature exceeding 37.2°C (99°F) due to the action of pyrogens.

• Mechanism: Pyrogens reset the hypothalamic thermostat, facilitating a higher temperature conducive to combating pathogens.

• Sources of Pyrogens: Can originate from pathogens or be produced by the body (e.g., interleukin-1, interferons).

• Benefits of Fever:

  • Inhibits pathogen reproduction.

  • Enhances the effectiveness of interferons.

  • Increases metabolic rates, improving the speed of immune reactions and recovery.

Adaptive (Acquired) Immunity

• Definition: A type of immunity that is not present at birth but is acquired through exposure to specific antigens or by receiving antibodies.

Types of Adaptive Immunity

1. Active Immunity:

   • Mechanism: The body actively produces antibodies in response to an antigen exposure or vaccination.

   • Examples:

     • Natural Exposure: Encountering antigens in the environment (e.g., through infections).

     • Artificial Exposure: Vaccinations (e.g., COVID vaccine).

2. Passive Immunity:

   • Mechanism: Antibodies are provided directly rather than being produced by the body.

   • Examples:

     • Naturally Acquired: Maternal antibodies transferred to a fetus via the placenta or through breast milk.

     • Artificially Acquired: Antibody infusions (e.g., rabies shots, Regeneron for COVID).

Immunity Types Breakdown

• Innate Immunity:

  • Present at birth, non-specific, genetically determined. No previous exposure needed.

  • Components include physical barriers, phagocytes, complement proteins, interferons, fever, inflammation.

• Adaptive Immunity:

  • Not present at birth, requires antigen exposure for antibody production.

  • Divided into active (antigen exposure or vaccination) and passive (direct antibody transfer).

Lymphocyte Production (Lymphopoiesis)

• Definition: Production of lymphocytes in the bone marrow, thymus, and lymphoid tissues.

• Classes of Lymphocytes:

  • T Cells: 80% of lymphocytes, includes various types:

  1. Cytotoxic T Cells: Attack infected or foreign cells.

  2. Helper T Cells: Stimulate B and T cell functions.

  3. Regulatory T Cells: Moderate immune responses.

  4. Memory T Cells: Respond more quickly to re-encountered antigens.

  • B Cells: 10-15% of lymphocytes, become plasma cells that produce antibodies.

  • Natural Killer Cells: 5-10% of lymphocytes, destroy infected cells by secreting perforins to disrupt target cell membranes.

Conclusion

• Understanding the distinctions between innate and adaptive immunity is essential as students progress to more complex immunology topics. Mastering these concepts and mechanisms provides a solid foundation for further studies in the field.