Definition: Abnormal immune response to allergens or antigens.
Types of Hypersensitivity:
Type I: Immediate hypersensitivity (e.g., Hay fever,Anaphylaxis)
Mechanism:
1st Exposure: Immune response results in increased IgE & mast cell loading.
2nd Exposure: Mast cell-IgE-antigen complex triggers mast cell degranulation. (making IgE way faster, loading mast cells causing it to degranulate, causing release of histamine, causing swelling.)
Phases:
Early Phase: Systemic histamine release.
Late Phase: Chemotaxis to eosinophils/neutrophils; release of leukotrienes, prostaglandins, and platelet activating factors.
Symptoms: Mild asthma, severe anaphylaxis, hives, rash, conjunctivitis, blocked airway, wheezing, rhinitis, shock, vomiting, diarrhea.
Type II: Antibody-mediated cytotoxicity.
Mechanism:
Antibodies bind to surface of cells (e.g., RBCs, basement membranes-glomeruli).
Causing autoimmune diseases
Trigger cell destruction through:
K cells,
Complement activation (MAC),
Phagocytic cells.
Type III: Immune complex mediated hypersensitivity.
Definition: Aggregation of antibodies and antigens forming emboli-like immune complexes.
Consequences: Deposits in blood vessels lead to microthrombi and inflammation; can cause arthritis and pneumoconiosis.
Type IV: Cell-mediated, delayed type hypersensitivity.
Mechanism: Helper T-cells stimulate cytotoxic T cells, macrophages, and K/NK cells. (T-cells can kill a cell)
Related Conditions: Chronic infections like tuberculosis (from microbacterium) and leprosy; includes tuberculin test as a diagnostic tool.
Things that take awhile to see exposure and response
Types:
Primary Immune Deficiencies:
Genetic disorders affecting the immune system.
B-cell deficiencies: Hypogammaglobinemia (B-cells aren’t producing antibodies), often sex-linked.
Associated with “bubble boy” individuals must live in a sterile environment to avoid infections. (most likely in girls)
T-cell deficiencies:
DiGeorge syndrome (thymus dysfunction).
SCID (Severe Combined Immunodeficiency), both T and B cells deficient leading to opportunistic infections (similar to AIDs).
Secondary Immune Deficiencies:
Results from environmental factors:
Age (thymus atrophy leads to less T cell activation).
Poor diet (low protein, zinc deficiency).
Diabetes.
Stress and immunosuppressive drugs.
Pathogen: HIV (HIV-I & HIV-II).
Transmission: Through fluids with high lymphocyte counts. (how many T-cells in that fluid)
Course of Disease:
Acute Phase: Antibody response, swollen lymph nodes, fatigue, diarrhea.
Full-blown AIDs: T-cell count drops below 200/mm3 leading to opportunistic infections (e.g., Kaposi's sarcoma, lymphoma, pneumocystis pneumonia, cryptosporidium, toxoplasmosis).
Characteristics:
Affect multiple organs or single organs.
Multifactorial origin; more prevalent in women than men.
Example: Systemic Lupus Erythematosus (SLE).
Prevalence: 1 in 700 women.
Diagnosis: Requires 4 out of 11 criteria; primarily targets multiple organ systems and presents positive anti-nuclear antibodies directed against nuclear components.
Involves loss of self-tolerance resulting in B-cell dysfunction; mainly Type III immune complex-mediated hypersensitivity and secondary Type II antibody-mediated cytotoxicity.
look at SLE?? SLIDE 21