homologous portion of CRl, an observation that is 
reminiscent of mutation and evolution in repeated 
genes (concerted or horizontal evolution) and sup- 
ports the hypothesis that the CRl polymorphic 
variants were generated by unequal crossing-over 
in this region. 
B. Decay-accelerating factor. DAF is a cell surface 
glycoprotein that protects cells from autologous 
complement-mediated lysis. DAF is one of the first 
phosphatidylinositol-linked molecules to be de- 
scribed on human T cells. Low levels of DAF were 
found to be expressed on a majority of freshly iso- 
lated human T cells, and DAF expression rapidly in- 
creased after T cell activation by mitogens. More- 
over, antibodies to DAF induced T cell proliferation 
if the cells are costimulated with phorbol esters. 
T cell mitogenesis was largely dependent on the 
phosphatidylinositol-linked form of DAF, because 
removal of DAF by a phosphatidylinositol-specific 
phospholipase C eliminates anti-DAF-induced T cell 
proliferation. These studies suggest that DAF on the 
surface of T cells may not only serve to afford pro- 
tection from autologous complement but may also 
function to transmit signals that induce T cell acti- 
vation. 
C. Membrane cofactor protein of complement. 
MCP is a C3-binding glycoprotein with a character- 
istic, relatively broad, two-band {M 63,000 and 
55,000) pattern by SDS-PAGE analysis. A rabbit 
polyclonal antibody was produced to the purified 
protein, and this reagent was employed to analyze 
the distribution of MCP on human peripheral 
blood cells. Flow cytometric analysis indicated that 
MCP is unimodally present on all platelets, granu- 
locytes, T helper lymphocytes, T suppressor/cyto- 
toxic lymphocytes, B lymphocytes, natural killer 
cells, and monocytes. It is not present on erythro- 
cytes. The presence of MCP on granulocytes was 
unexpected, and further evaluation indicated that 
PUBLICATIONS 
MCP of granulocytes has both structural and func- 
tional differences compared with MCP of platelets 
and mononuclear cells. To determine further its tis- 
sue distribution, surface-labeled human fibroblast, 
epithelial, and endothelial cells and cell lines were 
assessed for the presence of MCP by C3 affin- 
ity chromatography and by immunoprecipitation. 
These cells and cell lines all expressed MCP The 
wide tissue distribution of MCP supports the con- 
cept that this protein is important in the protection 
of host cells from complement-mediated damage. 
Also, the expression of MCP was found to be mod- 
ulated by SV40 transformation of two fetal fibro- 
blast lines. Transformation led to a 5- to 10-fold 
increase in expression as well as a preferential ex- 
pression of the lower molecular weight species, 
suggesting that viral infection can manipulate the 
regulation of this host regulatory protein. 
Biosynthetic and biochemical analyses indicated 
that the two forms of MCP were similar and that 
both contained N- and O-linked sugars. Pulse-chase 
experiments demonstrated approximately equal 
quantities of two precursor forms, with molecular 
weights of 41,000 and 43,000. The lower molecular 
weight precursor chased with a ^^^^ of 90 min, while 
the higher molecular weight precursor chased with 
a of 30 min. These experiments indicate that 
the two forms of MCP are structurally similar and 
are probably derived from two distinct precursors. 
They also suggest that variations in the rate of pro- 
cessing of two intracellular precursors may account 
for the dijBferential expression of the mature forms. 
Molecular analysis of these two precursor and ma- 
ture forms of MCP should be informative relative to 
the structural basis for this dififerential processing 
of two highly homologous precursor proteins. 
Dr. Atkinson is also Professor of Medicine and of 
Microbiology and Immunology at Washington Uni- 
versity School of Medicine and Physician at Barnes 
Hospital, St. Louis. 
Articles 
Atkinson, J. P 1988. Complement deficiency. Predisposing factor to autoimmune syndromes. Am J Med 85:45- 
Atkinson, J. P, Levitt, R., and Crouch, E. 1989. Migratory polyarthritis, pulmonary nodules, and chest pain in a 
60 year old man. Am J Med 86:209-215. 
Ballard, L.L., Bora, N.S., Yu, G.H., and Atkinson, J. P 1988. Biochemical characterization of membrane cofactor 
protein of the complement system, f Immunol 141:3923-3929. 
Continued 
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