Host response

Host Response to Infection

  • Immunology: Study of the immune system and the immune response.

  • Immunogen: Any substance capable of inducing an immune response (humoral, cellular, or both).

  • Antigen: Substance recognized by specific antibodies or T cells, serving as a target for the immune response.

  • Immunity: Ability to guard against diseases caused by microbes, toxins, and pollutants. Susceptibility refers to lack of immunity.

  • Two Types of Immunity:

    • Innate Immunity: Present from birth, provides first-line defenses (e.g., skin, mucous membranes) and second-line defenses (e.g., natural killer cells, phagocytes, inflammation).

    • Adaptive Immunity: Acquired after exposure to an antigen; improves on repeated exposure and is antigen-specific.

Innate Immunity

  • Exists from the start of life without prior exposure to antigens.

  • First-line Defenses:

    • Skin and mucous membranes (non-specific barriers).

  • Second-line Defenses:

    • Natural killer cells, phagocytes, inflammation, fever, antimicrobial substances.

Adaptive Immunity

  • Third Line of Defense:

    • Known as Acquired Immunity; occurs after exposure to antigens.

    • Characteristics:

      • Antigen-specific: Recognizes unique foreign substances.

      • Systemic: Immunity is not limited to the initial infection.

    • Lymphocytes: Blood cells that are integral to the immune response.

Arms of the Adaptive Defense System

  • Humoral Immunity: Mediated by antibodies present in body fluids, primarily involves B cells to neutralize threats outside cells.

  • Cellular Immunity: Involves living cells targeting infected or abnormal cells, primarily involves T cells.

Types of Adaptive Immunity

  • Active Acquired Immunity: Immunity gained from active production of antibodies through exposure to antigens.

  • Passive Acquired Immunity: Immunity acquired by receiving antibodies from another source (e.g., maternal antibodies).

The Immune System

  • Main Function: To defend against infections caused by various pathogens (viruses, bacteria, fungi, parasites).

  • Cells Involved:

    • B lymphocytes (B cells) and T lymphocytes (T cells).

  • Primary Lymphoid Organs: Thymus and bone marrow (sites for B and T cell development).

    • B cells mature in bone marrow, while T cells mature in the thymus.

  • Secondary Lymphoid Organs: Lymph nodes, spleen, mucosa-associated lymphoid tissues (tonsils, appendix, Peyer’s patches).

B Lymphocytes

  • Differentiate into plasma cells producing antibodies.

  • Present antigens and possess immunological memory (IgM & IgD on the surface).

T Lymphocytes

  • T Helper Cells (CD4+): Promote inflammation and antibody production.

  • Cytotoxic T Cells (CD8+): Recognize and kill infected, cancerous, or foreign cells.

Humoral Immunity

  • Involves both innate and adaptive processes via antibodies.

Antibodies

  • Globulin proteins (immunoglobulins) specific to the antigens.

Main Classes of Antibodies

  1. IgG: Predominant in secondary immune response; crosses the placenta; abundant in newborns; critical in chronic infections.

  2. IgM: Largest immunoglobulin; first antibody produced; present in acute infections; activates complement.

  3. IgA: Found in secretions; protects mucous membranes; prevents pathogen attachment.

  4. IgD: Marker for B cells; minimal known function; present in small amounts.

  5. IgE: Involved in allergy responses and defense against parasites; binds to mast cells and basophils.

Immune Responses

Primary Response

  • Occurs at the first encounter with an antigen.

  • Antibodies become detectable after 7-10 days; first are IgM, followed by IgG or IgA.

Secondary Response

  • Rapid and more intense response upon re-exposure to the same antigen characterized by memory cells.

  • IgG is produced in greater quantities than IgM.

Hypersensitivity Reactions

  • Type I: Immediate reactions mediated by IgE (allergic reactions).

  • Type II: Cytotoxic reactions mediated by IgG or IgM, leading to cell destruction.

  • Type III: Immune complex reactions causing localized inflammation and tissue damage.

  • Type IV: Delayed reactions mediated by T cells, leading to contact dermatitis and granulation responses.

Specific Hypersensitivity Types

  1. Type I: IgE-mediated immediate hypersensitivity (e.g., allergies, anaphylaxis).

  2. Type II: Cytotoxic hypersensitivity; involves antibody-mediated destruction of target cells.

  3. Type III: Immune complex-mediated tissue injury (e.g., serum sickness, Arthus reaction).

  4. Type IV: Delayed-cell mediated hypersensitivity (e.g., dermatitis from poison ivy).

Type 2 Hypersensitivity Mechanisms

    1. ADCC: Antibody-dependent cellular cytotoxicity.

    1. Complement-dependent lysis: Antibody activity causing cell damage via complement activation.

    1. Antibodies against cell receptors, e.g. Myasthenia Gravis.

Type 3 Hypersensitivity Mechanisms

  • Immune complex formation leading to inflammation and tissue damage, often seen in infections like malaria or hepatitis B.

Type 4 Hypersensitivity Mechanisms

  • 24-48 hour delay; examples include transplant rejection and contact dermatitis, demonstrating T cell involvement and response to sensitization.