The lesson presents an informative exploration of Type II and Type III Hypersensitivity Reactions. Type II Hypersensitivity Reactions are defined as autoimmune responses that can turn against the body in three ways: cellular destruction, inflammation, and cellular dysfunction. These are antibody-mediated responses where autoantibodies mistakenly target self-tissues. In cellular destruction, IgG and IgM antibodies bind to cells they're supposed to protect, leading to cell opsonization and subsequent phagocytosis by natural killer cells and macrophages, as seen in autoimmune hemolytic anemia and immune thrombocytopenia.
In inflammation, antibodies unintentionally deposit in tissues and activate compliment, causing tissue damage. This occurs in conditions like antibody-mediated glomerulonephritis and hyperacute transplant rejection. In cellular dysfunction, antibodies bind to cell receptors they're not supposed to, causing cells to malfunction, with examples such as Graves disease and myasthenia gravis.
Type III Hypersensitivity Reactions occur when immune complexes formed by IgG and IgM antibodies binding to antigens excessively deposit in tissues and blood vessels, leading to inflammation and tissue damage, characteristic of conditions like systemic lupus erythematosus, serum sickness, and the Arthus reaction.
Type II hypersensitivity, also known as antibody-dependent cytotoxic hypersensitivity, occurs when the immune system produces antibodies that mistakenly target and attack the body's own cells. It's characterized by antibody-mediated cell destruction, inflammation, and cellular dysfunction, and is typically associated with diseases like autoimmune hemolytic anemia, hyperacute transplant rejection, and Graves disease. On the other hand, Type III hypersensitivity, or immune complex-mediated hypersensitivity, involves the formation and deposition of immune complexes (antigen-antibody) leading to tissue damage and inflammation. Conditions under this reaction type include systemic lupus erythematosus, serum sickness, and the Arthus reaction.
Antibody-mediated glomerulonephritis is related to Type II hypersensitivity reactions as it is a condition where antibodies attack the glomeruli in the kidneys, causing inflammation and damage. These antibodies are specific to antigens found on the glomeruli, demonstrating the specificity typical of Type II reactions.
While both conditions involve kidney damage, the mechanisms of injury are different. Antibody-mediated glomerulonephritis, associated with Type II hypersensitivity, is driven by antibodies that bind to antigens on the glomerular basement membrane, leading to complement activation, inflammation, and tissue damage. In comparison, immune complex-mediated glomerulonephritis, related to Type III hypersensitivity, involves the deposition of circulating immune complexes in the glomeruli, triggering inflammation and potential glomerular injury.
Hyperacute transplant rejection is strongly associated with Type II hypersensitivity reactions. It is a rapid and severe reaction that occurs when pre-existing antibodies in a transplant recipient directly attack the transplanted tissue. The reaction is mediated by the binding of these antibodies to the donor's antigens, activating the complement system and leading to destruction of the transplanted tissue.