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Human cells express a battery of complement regulatory molecules which allow them to survive the continuous low-level complement attack which occurs on all cells exposed to plasma or other biological fluids. An explosion in our knowledge of the structures and mechanisms of action of these regulators has occurred in the last few years as a result of the molecular cloning of all but one (HRF) of the five known inhibitors. The three inhibitors of the C3/C5 convertases are functionally and structurally similar and have arisen from a common ancestor gene. The MAC inhibitors also appear to be functionally similar to each other but structural comparison awaits the cloning of HRF.

The relative importance of these inhibitors is likely to vary between tissues, but in the few instances where this has been studied in detail, CD59 and DAF appear to be the most important in allowing cells to survive …