Open AccessNormal C3b receptor (CR1) genomic polymorphism in patients with insulin‐dependent diabetes mellitus (IDDM): is the low erythrocyte CR1 expression an acquired phenomenon?
Author(s) -
RUUSKA P. E.,
IKÄHEIMO I.,
SILVENNOINENKASSINEN S.,
KÄÄR M.L.,
TIILIKAINEN A.
Publication year - 1992
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1992.tb06870.x
Subject(s) - diabetes mellitus , immunology , medicine , endocrinology , receptor , insulin dependent diabetes , insulin receptor , insulin , polymorphism (computer science) , biology , autoimmune disease , antibody , insulin resistance , gene , allele , genetics
SUMMARY Expression of the erythrocyte complement receptor (C3bR = CR1 = CD35) and its genomic polymorphism ( Hind III RFLP) was studied in a group of 80 patients with IDDM, 31 healthy siblings and 101 healthy blood donors. Defective CR1 expression was found in 26% of the patients with IDDM compared with 9% of the controls ( P <0.05) and 0% of the siblings. The CR1 gene polymorphism of the IDDM patients did not significantly differ from that of the controls. The presence of a 6.9 kb (L) CR1 gene fragment was associated with a low CR1 expression in the patients ( P <0.05) and especially in the controls ( P < 0.001). No significant association was found between the presence or absence of the HLA risk antigens for IDDM and CR1 expression. The results confirm that erythrocyte CR1 expression is genetically determined, but the CR1 deficiency associated with IDDM seems to be an acquired rather than a genetic phenomenon.