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Complement in type 1 (insulin-dependent) diabetes.

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G Senaldi, B A Millward, M J Hussein, D Pyke, R D Leslie, D Vergani. 1987. Complement in type 1 (insulin-dependent) diabetes.. https://doi.org/10.1007/bf00275751

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Inhibition of activation of human T lymphocytes by the complement C1 esterase inhibitor.

The major histocompatibility complex (MHC) class I molecules have been shown to be substrates to both of the complement C1 esterases. The effect of a C1 esterase-mediated cleavage of the MHC class I molecules on the activation process of lymphocytes was investigated by including the complement C1 esterase inhibitor (C1-Inh) in the medium during activation of human peripheral lymphocytes by staphylococcal enterotoxin A (SEA). The C1-Inh was shown to inhibit the activation of both CD4+ and CD8+ cells. No effect on activation of B lymphocytes was recorded, although the complement C1 complex was shown to bind to the B lymphocytes. Furthermore, the C1 complex bound to mononuclear cells was shown to be cleaved into molecular weights corresponding to the activated forms of the C1 esterases. The effect of the C1-Inh was much more pronounced at low cell density and the inhibition was not affected by the addition of interleukin-2 (IL-2). However, the inhibition was reduced when the cells were disturbed by addition of new portions of C1-Inh, 24 and 48 hr after the initiation of the activation. This indicates that the C1-Inh interference with the activation of T lymphocytes is mediated through a mechanism that requires some form of cell contact.

Complement C1

Assembly of the C1 complex.

The C1 complex of complement is a Ca(2+)-dependent complex protease comprising two loosely interacting subunits. C1q, the recognition subunit, is an hexameric protein with six peripheral globular domains, each connected through collagen-like "arms" to a central fibril-like "stalk". The catalytic subunit, C1s-C1r-C1r-C1s, is a Ca(2+)-dependent tetrameric association of two serine protease zymogens, C1r and C1s, that are sequentially activated by cleavage of a single peptide bond, upon binding of C1 to activators. Each monomeric protease is comprised of six structural motifs which form at least four domains, distributed in two functionally distinct regions, alpha (N-terminal) and gamma-B (C-terminal). The catalytic (gamma-B) regions of C1r and C1s are respectively located in the centre and at each end of the isolated tetramer, and the Ca(2+)-dependent C1r-C1s associations are mediated by the interaction (alpha) regions, which contain one Ca2+ binding site each. Physicochemical and electron microscopy studies indicate that the tetramer, which is highly elongated, folds into a more compact conformation upon interaction with C1q. Various models for C1 have been proposed, in which the tetramer either interacts with the outside part of the C1q arms (O- and W-shaped models), or is folded within the C1q arms (S- or 8-shaped models). These models are discussed in light of available information and in consideration of the structural requirements of C1 activation and function.

Complement C1