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Title of the item:

Correlations between serum factor B and C3b inactivator levels in normal subjects and in patients with infections, nephrosis and hypocomplementaemic glomerulonephritis.

Title :
Correlations between serum factor B and C3b inactivator levels in normal subjects and in patients with infections, nephrosis and hypocomplementaemic glomerulonephritis.
Authors :
Forristal, Judith
Iitaka, Kikuo
Vallota, Enrique H.
West, C. D.
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Subject Terms :
SERUM
INFECTION
GLOMERULONEPHRITIS
IMMUNE complex diseases
BIOMOLECULES
PATIENTS
PROTEINS
Source :
Clinical & Experimental Immunology; Apr1977, Vol. 28 Issue 1, p61-71, 11p
Academic Journal
In normal subjects, factor B and C3b inactivator (KAF) levels were linearly related (r = 0-71); factor B levels in subjects with low normal levels of KAF were significantly lower than in those with high normal levels of KAF. This relationship is postulated to be the result of modulation by the level of KAF of the availability of nascent, spontaneously formed, C3b, in turn responsible for a constant low-grade activation of the C3b feedback which determines in part the level of factor B. The correlation did not obtain in patients with infections; levels of KAF and, to a greater extent, factor B were elevated. In patients with glomerulonephritis and hypocomplementaemic because of in vivo classical pathway activation, KAF and factor B levels were also poorly correlated, presumably because many factors were influencing the levels of these proteins transcending the modulating effect of the concentration of KAF. On the other hand, in patients with nephrosis and with MPGN Type II, KAF and factor B levels were low but were directly correlated. In nephrosis the correlation may be the combined result of an equal rate of catabolism of these proteins and of modulation of factor B levels by the level of KAF as in normal subjects. In MPGN Type II, the correlation may reflect the fact, noted in in vitro studies, that with alternative pathway activation, the level of KAF influences the extent of factor B and C3 conversion to a greater extent than when complement is activated by the classical pathway. [ABSTRACT FROM AUTHOR]
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