• Type I (immediate or anaphylactic) hypersensitivity
      • Immunoglobulin E (IgE) antibody production by IgE B cells is stimulated by antigen. (MCQ)
      • The IgE antibody is then bound to the Fc receptors of basophils and tissue mast cells. . (MCQ)
      • On subsequent exposure, antigen (allergen) reacts with bound IgE antibody complement is not involved in this process. (MCQ)
      • results in cytolysis and degranulation of basophils or tissue mast cells . (MCQ)
      • This reaction requires bridging (cross-linking) of adjacent IgE molecules on the mast cell surface.
      • Degranulation results in histamine release, which increases vascular permeability. . (MCQ)
      •  Chemotactic substances recruit eosinophils, result in tissue and peripheral blood eosinophilia. . (MCQ)
      • Clinical examples
        • Allergic or atopic reactions . (MCQ)
        • seasonal rhinitis (hay fever)
        • allergic asthma. (MCQ)
        • urticaria (hives) . (MCQ)
        • Systemic anaphylaxis (anaphylactic shock), . (MCQ)
          • Rapid onset of urticaria, bronchospasm, laryngeal edema, and shock
          • Occur after exposure to an offending antigen is characteristic.
        • Angioedema . (MCQ)
          • acute edema of cutaneous or mucosal structures
          • most commonly involve the lips and eyelids
          • Laryngeal edema can occur and be life threatening.
          • Hereditary angioedema(MCQ)
            • caused by deficiency of C1 esterase inhibiter (MCQ)
            • not a manifestation of type I hypersensitivity. (MCQ)
            • Serum C4 is low and other complement components, such as C3, are consumed. (MCQ)
    • Type II (antibody-mediated or cytotoxic) hypersensitivity
      • Complement-fixing antibodies
        • react directly with antigens that are integral components of the target cell.
        • The interaction of complement with the cell surface results in cell lysis and destruction.
      • Serum complement is characteristically decreased. (MCQ)
      • The antigens involved are usually localized to tissue basement membranes or blood cell membranes.
      • Clinical examples include
        • warm antibody autoimmune hemolytic anemia (MCQ)
        • hemolytic transfusion reactions(MCQ)
        • hemolytic disease of the newborn (erythroblastosis fetalis), (MCQ)
          • antigens are components of red blood cell membranes
        • Goodpasture syndrome (antiglomerular basement membrane antibody disease), (MCQ)
          • pulmonary alveolar and glomerular basement membranes are affected.
        • Antibody-dependent cell-mediated cytotoxicity (ADCC) (MCQ)
          • Antibody reacts directly with integral surface antigens of targeted cells.
          • The free Fc portion of the antibody molecule reacts with the Fc receptor of a variety of cytotoxic leukocytes, most importantly NK cells. (MCQ)
          • Monocytes, neutrophils, and eosinophils, also bear Fc receptors and can participate in ADCC.
          • The target cells are killed by the Fc receptor-bound cytotoxic leukocytes.
          • Complement is not involved. (MCQ)
    • Type III (immune complex) hypersensitivity(MCQ)
      • Exogenous antibody produced in response to exposure to antigen combines with antigen, resulting in circulating antigen-antibody complexes.
      • In contrast to type II hypersensitivity, the antigen is not an intrinsic component of the target cells. (MCQ)
      • Immune complexes are most often removed by cells of the mononuclear phagocyte system without adverse effect.
      • In other cases, insoluble aggregates of immune complex are deposited in vessel walls or on serosal surfaces or other extravascular sites
      • The immune complexes bind complement, which is highly chemotactic for neutrophils.
      • The neutrophils release lysosomal enzymes, resulting in tissue damage
      • tissue damage can also result from  other substances released by neutrophils, including prostaglandins, kinins, and free radicals.
      • Serum complement is decreased. (MCQ)
      • Hageman factor (factor XII) is also activated(MCQ)
      • It causes
        • further activation of the intrinsic pathway of coagulation resulting in thrombosis in nearby small vessels
        • activation of the kinin system, resulting in vasodilation and edema.
        • Platelet aggregation and microthrombus formation
        •  leads to the release of vasoactive amines from platelet-dense granules.
    • Clinical examples
      • Serum sickness (MCQ)
        • a systemic deposition of antigen-antibody complexes in multiple sites
        • occur especially the heart, joints, and kidneys.
      • Systemic lupus erythematosus (MCQ)
      • Arthus reaction (MCQ)
        • a localized immune complex reaction that occurs when exogenous antigen is introduced, either by injection or by organ transplant, in the presence of an excess of preformed antibodies. (MCQ)
      • Polyarteritis nodosa (MCQ)
        • a generalized immune complex disease especially involving small- and medium-sized arteries.
      • Immune complex-mediated glomerular diseases include (MCQ)
        • poststreptococcal glomerulonephritis
        • membranous glomerulonephritis
        • lupus nephropathy.
    • Type IV (cell-mediated) hypersensitivity
      • Delayed hypersensitivity
        • The T-cell receptor of CD4+ lymphocytes interacts with the antigen, presented by macrophages, and with HLA class II antigens on macrophages
        • result in stimulation of antigen-specific CD4+ memory T cells. (MCQ)
        • On subsequent contact with antigen, the CD4+ memory T cells proliferate and secrete cytokines.
        • IL-2 and other cytokines secreted by the CD4+ T cells recruit and stimulate the phagocytic activity of macrophages. (MCQ)
    • Examples
      • tuberculin reaction
        • a localized inflammatory reaction
        • initiated by the intracutaneous injection of tuberculin
        • marked by proliferation of lymphocytes, monocytes, and small numbers of neutrophils
        • shows a tendency toward cellular accumulations about small vessels (perivascular cuffing). (MCQ)
        • Induration (hardening) results from fibrin formation.
      • Contact dermatitis 
        • may result from either delayed hypersensitivity or direct chemical injury to the skin.
      • Cytotoxic T lymphocyte–mediated cytotoxicity (MCQ)
        • direct CD8+ T cell–mediated killing of target cells
        • typically occur with  tumor cells or virus-infected cells
        • Specific target cell antigen is recognized by the T-cell receptor of CD8+ lymphocytes.
        • Target cell HLA class I antigens recognized as self-antigens are also required. (MCQ)
        • Cytokines are not involved. (MCQ)
    • Type V hypersensitivity,
      • Reaction of anti-receptor antibodies with cell-surface receptor protein(MCQ)
      • This is a variant of type II hypersensitivity
      • reaction of thyroid-stimulating immunoglobulin with the thyroid-stimulating hormone (TSH) receptor of thyroid follicular cells in Graves disease. (MCQ)
      • In Graves disease.
        • the antigen-antibody reaction mimics the effect of TSH on the follicular cells
        • results in glandular hyperplasia and hyperproduction of thyroid hormone with clinical hyperthyroidism.

    IgE mediated Type I hypersensitivity
    Type-I Hypersensitivity: IgE Mediated [HD Animation]
    See an organised list of all the animations
    Type-II Hypersensitivity: Cytotoxic Type [HD Animation]
    Hypersensitivity Reactions & Disorders (Types 1, 2, 3, 4)
    Hypersensitivity, Reactions, &, Disorders, (Types, 1,, 2,, 3,, 4), Findings, symptoms, findings, causes, mnemonics, review, what is, video, study, Rapid Review, Clinical presenation, First Aid, for, USMLE, Step 1, images, wiki, define, wikipedia, 2013, videos, exam, prep, easy, What is usmle, mnemonic, causes,
    Type 1 Hypersensitivity (Type I)
    Type-IV Hypersensitivity: Delayed Type [HD Animation]
    Delayed Type IV Hypersensitivity
    Type-III Hypersensitivity: Immune Complex Type [HD Animation]