Immune System Study Notes

Immune System Overview

  • The immune system is divided into 2 branches:

    • Innate Immunity

    • Adaptive Immunity

Innate Immunity (Chapter 14)

Definition

  • Innate immunity is referred to as "innate" because it is available immediately at birth.

Characteristics

  1. Nonspecific responses:

    • Members of innate immunity can attack a wide range of pathogens (e.g., bacteria, viruses).

    • Example: A phagocyte can eat and destroy various microbes, indicating its nonspecific capability.

    • The term "nonspecific" should not imply attacking self-cells.

  2. Figure Reference: (Refer to Figure highlighting components of innate immunity as 1st & 2nd lines of defense)

Adaptive Immunity (Chapter 15)

Definition

  • Also known as acquired immunity, termed adaptive in modern immunology.

Major Components

  1. B Cells:

    • Primary function: Produce antibodies (definition pending further notes).

  2. Antibodies:

    • Proteins produced by B cells that attach to specific chemicals known as antigens (definition pending).

    • Binding of antibodies to antigens initiates a variety of immune responses (expanded discussion to follow).

  3. T Cells:

    • Two types:

      • Helper T Cells (TH): Act as conductors, initiating and coordinating various immune responses.

      • Cytotoxic T Cells (TC): Target and kill infected cells and cancerous cells (definition of cytotoxic: deadly/harmful).

    • Detailed discussion on B cells, antibodies, and T cells in Chapter 15.

1st Line of Defense

Components

  1. Physical and Chemical Barriers:

    • Skin:

      • Intact skin serves as the first barrier by preventing entry of most microbes.

      • The outer layer of skin sloughs off, carrying microbes away with exfoliated skin cells.

    • Mucus Membranes:

      • Protect orifices and line various tubular structures within the body such as the respiratory and gastrointestinal tracts.

  2. Figure Reference: Refer to Figures 14.3 & 14.4 on pages 362 & 363 for additional physical and chemical barriers.

White Blood Cells (WBC)

Overview

  • Importance of learning the names and functions of specific leukocytes.

  • Memorization of leukocyte types outlined in the subsequent table is crucial (visual aspects of leukocytes not necessary for this unit).

Major Types of Leukocytes and Their Functions (Table 43.1)

  1. Monocyte:

    • Differentiates into a macrophage when entering damaged tissue from the blood.

  2. Macrophage:

    • Acts as a phagocyte that engulfs infected cells, pathogens, and cellular debris in damaged tissues; aids in activating lymphocytes as part of the immune response.

  3. Neutrophil:

    • A phagocyte that engulfs pathogens and tissue debris in damaged tissues.

  4. Eosinophil:

    • Secretes substances that kill eukaryotic parasites, such as helminths (worms).

  5. Lymphocyte:

    • Main subtypes include NK cells (natural killer cells), B cells, plasma cells, helper T cells, and cytotoxic T cells.

    • Functions in both innate and adaptive immunity; NK cells kill virus-infected cells and some cancerous cells.

  6. Basophil:

    • Located in the blood; responds to IgE antibodies during allergic reactions by secreting histamine to stimulate inflammation.

Phagocytosis

Overview

  • Macrophages and neutrophils are phagocytes.

Steps in Phagocytosis

  1. Chemotaxis of Phagocyte to Microbes (Initiated by chemical signals, leading to pseudopods moving towards microbes).

  2. Adherence: Phagocyte binds to the microbe.

  3. Ingestion of Microbes:

    • Formation of a phagosome that engulfs the microbe.

  4. Fusion: Combining phagosome with lysosomes.

  5. Killing of Microbes: Enzymatic and chemical processes kill the ingested microbes.

  6. Elimination: Waste products are discharged via exocytosis.

Inflammation

Four Hallmarks of Inflammation

  1. Redness

  2. Heat

  3. Swelling

  4. Pain

  • Inflammation is primarily a local response to infection. If it becomes systemic, it can be life-threatening.

Steps of Inflammation

  1. Following infection, damaged cells and nearby phagocytes release inflammatory chemicals. Histamine is a key component to memorize as it stimulates inflammation.

  2. Vasodilation occurs:

    • Blood vessels widen (increased diameter).

    • Blood vessels become more porous (increased permeability).

  3. Leakage of fluid occurs, delivering antimicrobial chemicals to the site of infection.

  4. Leukocytes migrate through blood vessels to the infected tissue.

  5. Clotting: Local blood vessels aid in preventing pathogens from entering the bloodstream.

  6. Tissue Repair: Active recuperation of affected areas, but further detail is reserved for Anatomy & Physiology (A&P) study.

Fever

Definition

  • An increase in body temperature, referred to as pyrexia (from Greek "pyro" meaning fire).

Mechanism

  1. Chemicals secreted by phagocytes interact with the hypothalamus, which serves as the temperature control center in the brain.

  2. The hypothalamus releases prostaglandin, adjusting the hypothalamic thermostat.

  3. Physiological responses occur, such as shivering and increased metabolic activity, raising body temperature to the new set point.

Benefits of Fever

  1. Interferes with the growth of certain microbes (dependent on specific temperature sensitivity).

  2. Enhances the efficacy of specific immune responses (examples noted in literature).

Controversy Regarding Fever Management

  • Discussion on the merits of allowing a fever to run its course within safe parameters versus the immediate need to mitigate fever-related risks.

Complement Cascade

Overview

  • Complement: A series of antimicrobial proteins found in the blood, labeled C1 – C9 (the numbering corresponds to their discovery rather than their functional order).

  • There are 3 pathways for complement activation, two of which will be discussed here.

Classical Pathway of Complement Activation

  1. Antibodies bind to antigens on the microbe surface.

  2. C1 binds to the antibodies and becomes activated, leading to the formation of C3 convertase.

  3. C3 convertase cleaves C3 into C3a and C3b.

  4. C3b: Functions as an opsonin, which enhances phagocytosis by binding to microbes, facilitating adherence by phagocytes.

    • Introduction of the term opsonization: Enhancement of phagocytosis via opsonin interaction with phagocyte receptors.

  5. Cleavage of C3b further leads to the formation of Macrophage Attack Complex (MAC) which causes lysis of the microbe.

  6. Release of histamine-inducing agents bind to mast cells similarly to basophils, promoting inflammation.

Alternative Pathway of Complement Activation

  • Activates through the binding of blood proteins (factors B, D, and P) along with C3 to the microbe surface.

  • This pathway can be initiated immediately post-infection, unlike the classical pathway, which requires prior antibody production.

Type I Interferons (Alpha & Beta)

Importance

  • Alpha & beta interferons play a crucial role in the immune defense against viral infections.

Mechanism of Action

  1. An infected cell synthesizes viral components, prompting production of alpha and beta interferons.

    • These interferons aren't beneficial to the cell producing them (it is infected and doomed to die).

  2. Interferons are released and bind to neighboring uninfected cells, inducing the production of antiviral proteins (AVPs).

  3. As viruses from the originally infected cell spread to nearby cells, the AVPs become activated, destroying mRNA and stopping protein synthesis, thereby hindering viral replication.

  4. It’s essential to differentiate between interferon (which signals healthy cells) and AVP, which acts to prevent the virus from replicating.

Additional Note

  • Another type of interferon, gamma interferon, plays a different functional role and will not be discussed in this module.