Immune Disorders

Acknowledgement to First Nations Peoples

  • CQUniversity recognizes and acknowledges the important role First Nations peoples make to communities.

  • Values Australian Indigenous knowledge systems as an integral part of teachings.

Immune Function

Chapter 3: Immune Disorders

Learning Objectives (pp.33-34)

  • Compare cellular and humoral immunity.

  • Outline the roles of major antibody classes, immune cells, and cytokines in immune processes.

Immune Function

  • Immunity: The condition of being resistant to infection by a specific pathogen.

    • Body Defences: Protection against foreign cells, organisms, and non-living particles.

    • Recognition of Antigens: Triggers an immune response.

    • Antigen: A substance/pathogen or foreign protein that causes antibody production by lymphocytes to defend the body.

    • Antibody: A protein (immunoglobulin) produced by lymphocytes in response to a harmful substance (antigen).

      • Functions: Binds to and inactivates specific foreign proteins (antigens).

Humoral Immunity

  • Acquired immunity where antibodies play a dominant role.

    • Defends against antigens and pathogens in body fluids.

    • B cells (lymphocytes) are stimulated to differentiate into plasma cells.

    • Secretion of antibodies (soluble proteins).

    • Binding of an antibody to its target antigen leads to the destruction of the target invader.

Active and Passive Humoral Immunity

  • Active Immunity: Establishes immunological memory.

    • Naturally Acquired: Infection; contact with the pathogen.

    • Artificially Acquired: Vaccine; exposure to dead or attenuated pathogens.

  • Passive Immunity: Does not establish immunological memory.

    • Naturally Acquired: Antibodies passed from mother to fetus via placenta; or to infant in her milk.

    • Artificially Acquired: Injection of exogenous antibodies (gamma globulin).

Cellular Immunity

  • Acquired immunity in which T cells (T lymphocytes) play a dominant role.

    • Cytotoxic T cells: Defend against abnormal cells and pathogens inside cells through direct cellular attack.

    • Helper T cells: Stimulate T cell and B cell responses.

    • Activate B cells before they can produce antibodies.

    • Regulatory T cells: Moderate the immune response.

    • Memory T cells: Respond to antigens they have previously encountered; produce identical copies of lymphocytes to fend off invaders.

Cellular and Humoral Immunity

  • Humoral Immune Response: Stimulates adaptive immune response upon first exposure to an antigen.

  • Cell-mediated Immune Response: Involves antigen-presenting cells, stimulates helper T cells and cytotoxic T cells, leading to the production of memory cells and active immune cells.

    • Defends against extracellular pathogens in body fluids by binding to antigens.

    • Defends against intracellular pathogens and cancer by binding to and lysing infected or cancer cells.

CD4 and CD8 T Cells

  • CD4 T cells: Help activate B cells, other T cells, and macrophages; direct adaptive immune response.

  • CD8 T cells: Destroy cells harboring foreign substances.

Immunoglobulins (Ig)

  • IgG: Most abundant (80-85%); crosses the placenta.

  • IgM: First antibody produced during primary response.

  • IgA: Present in saliva and secretions.

  • IgD: Functions as a B-cell antigen receptor.

  • IgE: Involved in allergic reactions; defends against parasites.

Antibody Classes and their Functions

Table of Immunoglobulin Classes

  • IgM:

    • First immunoglobulin class secreted during primary response; indicates current infection.

    • Exists in monomer and pentamer forms; potent agglutinating agent.

  • IgA:

    • Exists as a dimer in secretions; prevents pathogens from attaching to epithelial surfaces.

  • IgD:

    • Functions as B cell receptor.

  • IgG:

    • Most abundant in plasma; major antibody in secondary and late primary responses; crosses placenta.

    • Triggers histamine release during allergic reactions.

  • IgE:

    • Levels rise during allergic attacks; low amounts in plasma.

Cells that Participate in Tissue Defences

Table of Immune Cells and Functions

  • Neutrophils: Phagocytosis, inflammation.

  • Eosinophils: Phagocytosis of antigen-antibody complexes; allergic response.

  • Mast Cells/Basophils: Inflammation coordination.

  • Macrophages: Phagocytosis, antigen processing and presentation, secretes cytokines.

  • Dendritic Cells: Antigen presenting and processing.

  • Lymphocytes:

    • NK Cells: Destruction of abnormal cells.

    • T Cells (CD8, CD4): Cytotoxic and helper functions, regulatory roles.

    • B Cells: Secrete antibodies, participate in humoral immunity.

    • Memory Cells: Await antigen reappearance.

Cytokines

  • Cytokines: Chemical mediators that enhance immune and inflammatory cell functions.

    • Aid in cell interactions to kill bacteria; active during inflammation.

    • Types of cytokines:

    • Interferon: Protects against viral infections.

    • Interleukins: Communicate among leukocytes, crucial for immune response.

    • Tumour Necrosis Factor (TNF): Induces pro-inflammatory effects.

    • Transforming Growth Factor (TGF): Promotes cell differentiation and division.

Table of Cytokine Functions

  • Colony Stimulating Factors (CSF): Stimulate granulocyte and macrophage differentiation.

  • Interferon: Inhibit viral replication, boost T-cell proliferation.

  • Interleukin: Involved in fever, immune cell proliferation, and tissue repair.

Review

  • Understanding of:

    • Humoral and cellular immunity.

    • Major antibody classes, immune cells, and cytokines in immune processes.

Immune Dysfunction

Chapter 3: Immune Disorders

Learning Objectives (pp.35-36)

  • Explain autoimmune diseases and provide examples of common autoimmune disorders.

  • Discuss immunodeficiency; distinguish between primary and secondary immunodeficiencies.

Autoimmunity

  • Autoimmunity: Development of antibodies against self-antigens.

    • Immune response against one's body tissues, viewed as foreign.

  • Self-tolerance: Mechanisms to prevent autoimmunity:

    • Apoptosis or inactivation of self-reactive B and T cells.

    • Suppression of sensitized T cells.

    • Physical barriers preventing immune access to privileged sites (e.g., brain).

  • Autoimmune Disease: Tissue damage caused by an autoimmune response.

Mechanism of Autoimmune Diseases

  • Disruption in suppression of sensitized T cells.

  • Breach of barriers at privileged sites or cross-reactivity with infectious agents.

  • Results in chronic inflammation and tissue damage leading to fibrosis.

Autoimmune Disorders

  • Caused by the immune system's inability to differentiate self from non-self.

  • Human Leukocyte Antigen (HLA) genes are critical in antigen presentation to T cells.

Immunodeficiency

  • Immunodeficiency: Conditions causing deficiency in immune cell production or function, increases susceptibility to infections/neoplasia.

  • Two types:

    • Primary Immunodeficiency: Affects immune system directly; includes humoral, cellular, and combined deficiencies.

    • Secondary Immunodeficiency: Result of environmental factors affecting immune function.

Primary Immunodeficiencies

Cellular Immunodeficiencies

  • Primarily affect T cells; characterized by poor T cell responsiveness.

    • DiGeorge Syndrome: Chromosome 22 deletion; underdeveloped thymus and other structures.

Humoral Immunodeficiencies

  • Affect B cell numbers and antibody production.

    • Selective IgA Deficiency: Increased risk for autoimmune conditions and allergies.

    • Common Variable Immunodeficiency (CVID): Issues with autoimmunity and inflammation.

    • Bruton's Agammaglobulinaemia: Affects B cell levels.

Combined Immunodeficiencies

  • Defects in stem cell development affect both T and B cells.

    • Severe Combined Immunodeficiency (SCID): Affected antibody and T/NK cell production.

Secondary Immunodeficiencies

  • Environmental Factors:

    • Stress: Corticosteroid release decreases immune function.

    • Malnutrition: Impairs production of immune mediators; lack of vitamins and minerals.

    • Drug Treatments: Corticosteroids and chemotherapeutics inhibit immune cell production.

    • Infections: E.g., HIV impacts immune function directly.

    • Cancer: Results in diminished immune response.

Human Immunodeficiency Virus (HIV) and AIDS

Chapter 3: Immune Disorders

Learning Objectives (pp.39-41)

  • Describe the pathophysiology, clinical manifestations, and management of HIV/AIDS.

HIV Overview

  • Human Immunodeficiency Virus (HIV): Virus leading to AIDS.

    • Directly targets helper T cells (CD4+).

    • Historical theory: Direct destruction of CD4+ cells leads to immunodeficiency.

    • Current theory: Chronic activation of the immune system results in T cell proliferation and shortened lifespan.

Aetiology of HIV Infection

  • Transmission routes include unprotected sex, mother-to-baby, or exposure to contaminated blood.

Pathophysiology of HIV

  • Infects CD4+ T cells, macrophages, and dendritic cells.

  • Progressive weakening of both cellular and humoral immune processes, leading to vulnerability to opportunistic infections.

Clinical Manifestations of HIV

  • Early stages may include fever, rash, swollen lymph nodes, sore throat; often asymptomatic.

  • Progression to AIDS characterized by weight loss, chronic diarrhoea, persistent fatigue, and opportunistic infections.

Opportunistic Infections

  • Common infections:

    • C. albicans: Fungal infection.

    • Toxoplasmosis: Protozoan infection.

    • Tuberculosis: Bacterial infection.

  • Increased cancer risk includes Kaposi's sarcoma.

Management of HIV

  • Focus on maximizing health and maintaining immunocompetence through:

    • Combination Antiretroviral Therapy: Regulates viral load and supports immune function; be cautious of resistance and side effects.

    • Good Nutrition and healthy lifestyle choices.

    • Vaccinations: Against hepatitis and influenza as suited to immunosuppression levels.

    • Antibiotics and Antifungal agents for opportunistic infections.

Hypersensitivity Reactions

Chapter 3: Immune Disorders

Learning Objectives (pp.42-46)

  • Identify the four types of hypersensitivity reactions and examples of specific conditions associated with these reactions.

Hypersensitivity Overview

  • Hypersensitivity: An exaggerated immune response to harmless antigens leading to tissue damage.

  • Types differentiated by response speed, immune mediation, and antibody involvement.

Types of Hypersensitivity Reactions

Type I Hypersensitivity Reactions

  • Mediated by IgE.

  • Common reactions like allergies, anaphylaxis, and localized responses (e.g., skin rashes).

  • Mechanism: Initial exposure triggers IgE antibody production; subsequent exposure leads to mast cell degranulation and release of inflammatory mediators.

Type II Hypersensitivity Reactions

  • Tissue-specific, mediated by IgG and IgM.

  • Examples: Myasthenia gravis and blood transfusion reactions.

  • Mechanism: Antibodies bind to cell tissues, leading to immune cell recruitment and destruction of target cells.

Type III Hypersensitivity Reactions

  • Immune complex-mediated, mediated through IgG antibodies; prolonged inflammatory responses.

  • Examples: Systemic lupus erythematosus.

  • Mechanism: Antibodies bind soluble antigens, forming complexes that deposit in tissues, triggering inflammation.

Type IV Hypersensitivity Reactions

  • Cell-mediated, involving T cells.

  • Examples: Contact dermatitis and granulomatous diseases.

  • Mechanism: Initial exposure sensitizes T cells; re-exposure triggers an inflammatory response by activating phagocytes.

Review

  • Understanding of:

    • The four types of hypersensitivity reactions.

    • Specific conditions associated with these reactions.

References

  • Bullock, S. & Hales, M. (2024). Principles of Pathophysiology.

  • Carlson, D. & Clapperton, R. (2025). Pathophysiology and Pharmacology for Nurses.

  • Craft, J.A., et al. (2023). Understanding Pathophysiology.

  • Marieb, E.N. & Hoehn, K. (2023). Human Anatomy & Physiology.

  • Martini, F.H., et al. (2018). Fundamentals of Anatomy and Physiology.

  • Nath, J. (2023). Applied Pathophysiology: A Conceptual Approach.

  • Sorenson, M., et al. (2019). Pathophysiology.