No. Type II hypersensitivity results from the binding of antibodies to antigens on cell surfaces or extracellular matrices. This binding either results in 1) opsonization and phagocytosis, 2) complement activation, or 3) antibody-mediated inhibition or stimulation. Examples include Goodpasture syndrome and myasthenia gravis.
The damage done in lupus is primary the result of what type of hypersensitivity reaction?
No. Type IV or "delayed-type" hypersensitivity is a T-cell memory phenomena where T-cells respond to a previously encountered peptide antigen. As a result the T-cell secrete inflammatory cytokines that results in inflammation, macrophage activation, and cell injury. The reaction is commonly seen reactions to PPD (the TB test) and poison-ivy.
No. Type I is immediate hypersensitivity, where IgE molecules bound to Fc-receptors on mast cells are exposed to antigen, causing mast cell degranulation. This type of hypersensitivity is commonly seen in allergies (e.g. ragweed).
Yes. Much of the damage in Lupus results from the formation of antibody-antigen complexes that circulate and ultimately deposit in tissues such as the kidney and synovium.
No. There are only 4 types of hypersensitivity reactions.
