activation of the complement system is a group of blood proteins that mediate the specific antibody response; It is triggered by antigen-bound antibody molecules. (The only antibodies capable of binding are two units of IgG or one IgM. IgG4 cannot bind, but the other three IgG types can.) It is the binding of a specific part of the antibody molecule to the C1 component that initiates this pathway.
In this pathway, activation occurs independent of Antibodies; instead it occurs when complement proteins (B, D, and Properdin) bind to Endotoxins or Glycoproteins in the Cells of bacteria or Fungi
initiated by binding of the complex of mannose-binding lectin and associated serine proteases to arrays of mannose groups on the surface of a bacterial cell.
Cell-surface proteins on various cell types that recognize and bind complement proteins bound to antigens (chiefly C3b). Those on phagocytes facilitate the phagocytic engulfment of pathogens coated with complement.
process whereby opsonins make an invading microorganism more susceptible to phagocytosis
Membrane Attack Complex
(MAC) unique system that bilds up a lipophilic complex in cell membranes from several plasma protiens.
C1 Esterase Inhibitor (C1 Inhibitor)
deficiency of this causes hereditary angioedema by enhanced production of C2b and C4a which lead to increased vascular permeability, also down-regulates kallikrein -> treat by infusing a synthetic infusion of this protein
Decreased levels an be demonstrated in patients with hypocomplementemic urticarial vasculitis, severe combined immunodeficiency (SCID), or X-linked hypogammaglobulinemia.
measures the binding of immune complexes containing IgG1, IgG2, or IgG3 and IgM to the complement component C1q.
Acute-phase protein, elevated C3 can indicate an accute Inflammatory disease; depressed more in alternative pathway.
allotypes in cinjuction with specific human Leukpcyte antigens are markers for disease susceptibility.
deficiency of C5 is associated with increased susceptibility to bacterial infection and expressed as an autoimmune disorder.
proteins that stimulate the growth of B or T lymphocytes and activate specific components of the immune response
Cytokines that help cells to resist viral infection. Interferon-α (IFN-α) and interferon-β (IFN-β) are produced by leukocytes and fibroblasts respectively, as well as by other cells, whereas interferon-γ (IFN-γ) is a product of CD4 TH1 cells, CD8 T cells, and NK cells. IFN-γ acts principally to activate macrophages.
increase the expression of adhesion factors on endothelial cells to enable transmigration of leukocytes to sites of infection and reset the hypothalamic thermoregulatory cent, leading to increased body temperature.
IL-2 (formerly "T-cell growth factor")
increases cytoxic functions of T-Killer and NK cells; promotes production of perforins and IFN-y by thses cells.
IL-3 (formerly "multicolony colony-stimulation factor")
Promotes expansion of early blood cells that differentiate into all known mature cell types.
Secreted by TH 2 cells. Promotes differentiation of B cells. Enhances class switching to IgA. Stimulates production and activation of eosinophils.
A cytokine produced by many cell types, including activated mononuclear phagocytes, endothelial cells, and fibroblasts, that functions in both innate and adaptive immunity. Stimulates the synthesis of acute phase proteins by hepatocytes and stimulates the growth of antibody-producing B lymphocytes.
Tumor Necrosis Factor
Cytokine that mediates gram negitive infections. Recrutes wbc to infection and activates cells to irradicate microbes.
Stem Cell Factor
cytokine that interacts with tyrosine kinase membrane receptor, the protein product of the cellar oncogene c-kit. (c-kit ligand)
..., large group of small proteins involved in guiding white blood cells to sites where their functions are needed; have a central role in inflammatory responses
Liver proteins released during the active immune phase. They act as opsonins & enhance the inflammatory response.