Maternal-fetal interactions and disease

Article Abstract:

Remission or improvement of rheumatoid arthritis (RA) during pregnancy may be caused by differences in fetal and maternal HLA antigens. HLA antigens may play an important role in the development and progression of RA and other autoimmune diseases. Different types of HLA antigens are encoded by the genes of the major histocompatibility complex (MHC). The association between class II MHC antigens and certain diseases may be caused by different genetic abnormalities. Class I HLA antigens are found on the surface of the human placenta but class II HLA antigens are not. The mother's immune system does not attack the placenta although it is genetically different. A research study found that fetal-maternal differences in HLA antigens may occur in women who have remission or improvement of RA during pregnancy. Improvement may occur because maternal HLA-DQ antigens bind to subunits of fetal proteins. This prevents activation of maternal cells involved in the development and progression of RA.

Maternal-fetal exchange

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Maternal-fetal disparity in HLA class II alloantigens and the pregnancy-induced amelioration of rheumatoid arthritis

Article Abstract:

Remission or improvement of rheumatoid arthritis (RA) during pregnancy may be caused by differences in fetal and maternal HLA antigens. HLA antigens may play an important role in the development and progression of RA and other autoimmune diseases. Of 46 pregnancies among women with RA, 22 were characterized by remission of RA, 12 by improvement of RA and 12 by active RA. Fetal-maternal differences in HLA-DRB1, DQA and DQB antigens occurred in 76% of the pregnancies with remission or improvement of RA, compared with 25% of the pregnancies with active disease. A fetal-maternal difference was most likely to occur in the HLA-DQA antigen in women who had remission or improvement of RA during pregnancy. Remission or improvement of RA during pregnancy may be partially caused by an immune response against paternal HLA antigens by the mother.

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Relation of an interleukin-10 promoter polymorphism to graft-versus-host disease and survival after hematopoietic-cell transplantation

Article Abstract:

A variation in the gene for interleukin-10 called -592A is associated with a lower risk of graft-versus-host disease (GVHD) in people who receive a stem cell transplant, according to a study of 993 patients. Patients who had this gene variation were about half as likely to develop GVHD as those who did not. GVHD is a serious complication of stem cell transplants in which the transplant attacks the body of the recipient.

Health aspects, Complications and side effects, Genetic aspects, Genetic polymorphisms, Hematopoietic stem cell transplantation, Graft versus host reaction, Graft vs. host disease

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