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Page 1: Hypersensitivity Reactions

• Immediate Reactions

  • Develop within minutes to hours post-antigen exposure.

  • Includes Type I, Type II, Type III hypersensitivities.

  • Also known as anaphylactic hypersensitivity; commonly occur after allergen exposure.

  • Key components:

    • IgE: Involved in type I hypersensitivity response.

    • Mast Cells: Release histamine and other mediators upon activation.

    • Basophils: Similar function to mast cells, involved in allergic responses.

    • Eosinophils: Involved in combating parasites and contribute to allergic inflammation.

• Type I Hypersensitivity

  • Example: Urticaria (hives) characterized by wheal and flare.

  • Positive skin test shows wheal and flare at allergen application site.

  • Transfusion Reactions: Mediated by antibody-antigen interactions; small antigen-antibody complexes precipitate and deposit in tissues.

• Type IV Hypersensitivity

  • Cell-Mediated/Delayed Hypersensitivity: Involves Th1 cells and macrophages.

  • Skin Testing for Delayed Hypersensitivity: Mantoux method identifies previous exposure.

• Type I Hypersensitivity Testing (In Vivo Skin Tests)

  • Allergens induce IgE production which binds mast cells and basophils, causing degranulation and allergic symptoms.

• Clinical Examples of Type II Hypersensitivity

  • Hemolytic disease of the newborn (HDN).

  • Autoimmune hemolytic anemia.

• Type III Hypersensitivity

  • Small immune complexes with IgG or IgM precipitate in tissues.

  • Example: Tuberculosis test (PPD); a positive test shows induration.

  • Type II Hypersensitivity: IgG and IgM bind cell surface antigens causing cell damage or dysfunction through various mechanisms (complement lysis, opsonization, ADCC).

Page 2: Systemic Diseases and Diagnostic Testing

• Systemic Lupus Erythematosus (SLE)

  • Causes immune complex deposition and inflammation (neutrophils release enzymes leading to tissue injury).

  • Common symptoms: Skin rashes (80% of patients), butterfly rash is a key sign.

  • Laboratory Tests for SLE:

    • ANA Testing: Anti-nuclear antibodies are often present.

    • Fluorescent ANA Test:

      • Homogeneous pattern indicates antibodies to dsDNA, histones common in SLE.

      • Speckled pattern suggests anti-ENA antibodies, typical in SLE and scleroderma.

      • Nucleolar pattern indicates antibodies to RNA and RNP, seen mainly in scleroderma.

    • IIF with Crithidia luciliae: Detects antibodies against a circular organelle containing double-stranded DNA.

• Laboratory Testing for Rheumatoid Arthritis (RA)

  • ANAs present in approximately 40% of RA patients, commonly directed against RNP.

• Granulomatosis with Polyangiitis (Wegener's granulomatosis)

  • Organ-specific autoimmune disease, inflames small- to medium-sized blood vessels.

  • Commonly develops systemic disease affecting multiple organs.

  • Neutrophils activated by antibodies to cytoplasmic proteins like proteinase 3 cause vascular endothelial damage.

Page 3: Autoimmune Disorders

• Hashimoto's Thyroiditis (TPO, Tg antibodies present).

• Multiple Sclerosis (MS): Involves central nervous system's inflammation/damage.

• Goodpasture's Syndrome: Antibodies against glomerular basement membrane cause kidney and lung damage.

• Host-Microbe Relationships

  • Commensalistic Relationships: No harm or benefit to organisms involved.

• Illnesses of Acute Group A Strep Infection

  • Can cause upper respiratory tract infections leading to rheumatic fever or glomerulonephritis if untreated.

  • Poststreptococcal Glomerulonephritis: Follows strep skin or throat infections.

• Helicobacter Pylori Testing

  • CLOTest: Biopsy tissue tested for urease presence; indicates infection.

• Mycoplasma Pneumoniae: Known colloquially as “walking pneumonia.”

• Spirochete Diseases

  • Include Syphilis, Lyme disease, and Relapsing fever.

  • Stages of Syphilis:

    • Primary: Chancre development.

    • Tertiary: Severe symptoms arise—gummas, cardiovascular issues, neurosyphilis.

  • Laboratory Diagnosis of Syphilis:

    • Gram-positive cocci identified via microscopy.

    • Person-to-person transmission confirmed.

Page 4: Diagnostic Methods and Immune Responses

• Fluorescent Antibody Staining: Uses antibodies labeled to identify T. pallidum in microscopy.

• RPR Test: Cardioplipin antigen mixed with patient serum for diagnosis.

• Natural/Innate Immunity

  • Mechanisms include skin, WBCs, macrophages, and various secretions (tears, mucus, etc.).

• Haptens: Nonimmunogenic substances that require a carrier to incite an immune response.

• Immunoglobulin Across Placenta: Primarily IgG.

• B Cells: Produce humoral antibodies as part of acquired immunity.

• Hybridoma Technology: Combines cancerous cells with antibody-producing cells for sustained antibody production.

• MHC Class I: Present on all nucleated cells; involved in immune recognition.

• Immunoglobulin A (IgA): Present in mucosal secretions; important for immune response at mucosal surfaces (milk, saliva, tears).

Page 5: Adaptive Immune Response

• Humoral Immune Response

  • Involves B cells and plasma cells producing antibodies.

  • Th2 Cells: Produce IL-4, IL-10; key in antibody-related immunity and regulation regarding allergies and autoimmunity.

• Cytokines:

  • IL-1: Attracts immune cells and acts as an endogenous pyrogen.

  • IL-3/IL-7: Involved in hematopoiesis.

• Cell Signaling

  • Autocrine: Cytokines act on the cell that released them (e.g., IL-1β).

  • TGF-B: Regulates cell growth and limits activated cell expansion.

• Lymphocytes: Essential for recognizing distinct antigenic determinants.

• Erythropoietin (EPO): A cytokine used to treat severe anemia; affects hypothalamus to induce fever in response to infections.