MicroVue C4d EIA*

For Research Use Only in the United States. Not for use in diagnostic procedures.

The MicroVue C4d Enzyme Immunoassay measures the amount of C4d-containing fragments present in human plasma, serum and other biological or experimental samples.

Complement Component C4 is unique to the classical complement pathway. Classical pathway activation is triggered upon the binding of the C1q component of C1 to IgG or IgM containing immune complexes or other activating substances (retroviruses, certain bacteria, parasites, transformed cells, subcellular membranes, DNA and CRP/phosphorylcholine complexes). Binding of C1 to one of these activators results in the conversion of the C1s zymogen to an active proteolytic enzyme. Activated C1s can then cleave C4 at peptide bond 77 to yield C4a, an anaphylatoxin, and C4b. Both fragments have important functions in vivo. As an anaphylatoxin, C4a has a short half life and is bound by cells with the appropriate receptors. C4b mediates opsonization of target cells and can participate in the classical pathway convertase.

The expression of C4b activity is strictly regulated. C4b is rapidly cleaved by Factor I (with CR1 or C4 Binding Protein as cofactor). Cleavage by Factor I yields inactive C4b or C4bi. Further degradation by Factor I yields the fragments C4c and C4d.

C4d has been measured in human serum and plasma. The levels of C4d, normalized by the levels of native C4 can be significantly elevated in specimens obtained from patients with RA, HAE, SLE and chronic urticaria with hypercomplementemia. C4d levels may also be elevated in plasma from patients with a variety of humoral autoimmune diseases in which classical complement activation is known to occur. Because C4 is unique to the classical complement pathway, the C4d activation fragment of C4 is an excellent marker for classical complement pathway activation.

An EIA for the measurement of C4d -containing fragments in experimental samples.

References

Mold, C. Tamerius, J.D., et al., Complement activation during painful crisis in sickle cell anemia, Clinical Immunology and Immunopathology, 70:3,314-320, 1995.

Feucht, H.E., Felber, E, et al. Vascular deposition of complement split products in kidney allografts with cell mediated rejection, Clin Exp Immunol 86:464-470, 1991.

Manzi, S., Rairie, J. et al. Sensitivity and Specificity of plasma and urine complement split products as indicators of lupus disease activity, Arthritis and Rheumatism 39(7)1178-1188, 1996.

Jarvis, J., Taylor, H. Complement activation and immune complexes in children with polyarticular juvenille rhuematoid arthritis: a longitudinal study, J Rheumatology 21(6)1124-1127, 1994.

Aggarwaal, A., et al. Evidence for activation of the alternative complement pathway in patients with juvenille rheumatoid arthritis, Rheumatology 39:189-192, 2000.

Buyon, J,, Tamerius J. et al. Assessment of Disease activity and impending flare in patients with systemic lupus erythematosis, Arthritis and Rheumatism35(9)1028-1036, 1992.

Shaw, D., Rustagi, P. et al. Effects of Synthetic Oligonucleotides on human complement and coagulation, Biochemical Pharmacol 53(8)1123-1132, 1997.
 

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