Cutting Edge: Persistent Fetal Microchimerism in T Lymphocytes Is Associated with HLA-DQA1*0501: Implications in Autoimmunity
Author(s) -
Nathalie Lambert,
Paul C. Evans,
Tanya L. Hashizumi,
Sean Maloney,
Ted Gooley,
D E Furst,
J. Lee Nelson
Publication year - 2000
Publication title -
the journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.737
H-Index - 372
eISSN - 1550-6606
pISSN - 0022-1767
DOI - 10.4049/jimmunol.164.11.5545
Subject(s) - microchimerism , immunology , human leukocyte antigen , autoimmune disease , pathogenesis , autoimmunity , genotype , scleroderma (fungus) , major histocompatibility complex , allele , medicine , fetus , pregnancy , biology , immune system , gene , antigen , genetics , antibody , inoculation
The host's MHC genotype plays a critical role in susceptibility to autoimmune diseases. We previously proposed that persistent fetal microchimerism from pregnancy contributes to the pathogenesis of autoimmune diseases such as scleroderma. In the current study, we investigated whether the specific host MHC genotype is associated with persistent microchimerism among T lymphocytes in women with scleroderma and in healthy women. Fetal microchimerism among T lymphocytes was strongly associated with HLA DQA1*0501 of the mother (odds ratio (OR) = 13.5, p = 0.007, p corrected (pc) = 0.06) and even more strongly with DQA1*0501 of the son (OR = infinity; p = 0. 00002, pc = 0.0002). This is the first description of an association between persistent fetal microchimerism in maternal T lymphocytes and specific HLA class II alleles. Although the association was observed in both healthy women and in women with scleroderma, the finding suggests an additional route by which HLA genes might contribute to susceptibility to autoimmune disease.
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