Expression of IgG Fc receptor antigens in placenta and on endothelial cells in humans. An immunohistochemical study.

DD Sedmak, DH Davis, U Singh… - The American journal …, 1991 - ncbi.nlm.nih.gov
DD Sedmak, DH Davis, U Singh, JG Van de Winkel, CL Anderson
The American journal of pathology, 1991ncbi.nlm.nih.gov
Abstract Expression of leukocyte IgG Fc receptor (Fc gamma R) antigens by placenta,
endothelial cells (EC) of normal tissues, and ECs of kidney and skin from subjects with
immune complex diseases was studied immunohistochemically using anti-Fc gamma R
monoclonal antibodies (MAb). Monoclonal antibodies against all three leukocyte Fc gamma
R classes stained placental villous macrophages. Placental villous trophoblasts were
stained intensely by anti-Fc gamma RIII MAb 3G8, while both anti-Fc gamma RI (MAb 32) …
Abstract
Expression of leukocyte IgG Fc receptor (Fc gamma R) antigens by placenta, endothelial cells (EC) of normal tissues, and ECs of kidney and skin from subjects with immune complex diseases was studied immunohistochemically using anti-Fc gamma R monoclonal antibodies (MAb). Monoclonal antibodies against all three leukocyte Fc gamma R classes stained placental villous macrophages. Placental villous trophoblasts were stained intensely by anti-Fc gamma RIII MAb 3G8, while both anti-Fc gamma RI (MAb 32) and anti-Fc gamma RII MAbs IV3, KU79, CIKM5, 2E1, KB61, and 41H16) antibodies did not react with these cells. Anti-Fc gamma RII MAbs IV3, KU79, CIKM5, 2E1, KB61, and 41H16 immunostained placental villous capillary EC, in contrast to anti-Fc gamma RI MAb 32 and anti-Fc gamma RIII MAb 3G8, CLB-Granl, and B73. 1, which did not bind. Anti-Fc gamma RI MAb 32, anti-Fc gamma RII MAb IV3 and CIKM5, and anti-Fc gamma RIII MAb 3G8 did not react with the ECs of tonsil, liver, kidney, spleen, intestine, lung, or uterus. Similarly no EC staining was seen with these four MAbs in 14 skin and 14 kidney biopsies from subjects with immune-complex diseases. Fc gamma R antigens are expressed constitutively only by placental villous ECs and are not induced on nonplacental ECs by immune-complex-mediated diseases.
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