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Rheumatoid arthritis (RA) often ameliorates during pregnancy and flares postpartum, but the relationship of pregnancy and childbirth to RA prognosis is unclear. We examined RA severity for association with parity prior to RA onset and asked whether time from birth (latency) and/or the mother's HLA genotype influenced results. A cohort study was conducted of 222 women previously identified in a prospective study of newly diagnosed RA, who returned for follow-up evaluation a median of 8 years later. Stratified analyses using Mantel-Haenszel methods were conducted to evaluate 5 RA severity measures based on hand and wrist radiographs, physical exams, and Health Assessment Questionnaires for association with parity. Overall, we observed little evidence of altered risk of progression to severe RA in relation to pre-onset parity, adjusting for RA onset age and time to follow-up. Stratifying parous women who had only live births by latency (<15 years/15+ years) showed no difference in risk of severe RA compared to nulligravid women. Live birth deliveries were significantly protective for women with 0 but not for those with 1 or 2 copies of the RA risk-associated HLA-DRB1 shared epitope sequence for erosion score (RR 0.26 95% CI 0.09–0.89) and joint count (RR 0.28 95% CI 0.09–0.87). We observed little evidence of difference in severe RA by pre-onset parity overall. However, among women not predisposed to RA by possessing the risk-associated HLA genotype, parous women who had only live births had lower risk of progression to severe RA as measured by erosion score and joint count. [ABSTRACT FROM AUTHOR]

Microchimerism (Mc) refers to the harboring of a small number of cells (or DNA) that originated in a different individual. Naturally acquired Mc derives primarily from maternal cells in her progeny, or cells of fetal origin in women. Both maternal and fetal Mc are detected in hematopoietic cells including T and B cells, monocyte/macrophages, natural killer (NK) cells and granulocytes. Mc appears also to generate cells such as myocytes, hepatocytes, islet β cells and neurons. Here, the detrimental and beneficial potential of Mc is examined. The prevalence, diversity and durability of naturally acquired Mc, including in healthy individuals, indicates that a shift is needed from the conventional paradigm of ‘self versus other’ to a view of the normal ‘self’ as constitutively chimeric. [ABSTRACT FROM AUTHOR]

It is now well recognized that cells traffic in both directions between fetus and mother during pregnancy. Moreover, fetal cells have been found to persist for years, probably for a lifetime, in the circulation of healthy women. Harboring of cells from another individual at low levels is called microchimerism. Women have a predilection to autoimmune disease, and chronic graft-versus-host disease, a condition of human chimerism, shares similarities with some autoimmune diseases. The specific HLA genes of donor and host are known to be of central importance in graft-versus-host disease, and HLA class II genes are important in autoimmune disease. Considered together, these observations led to the hypothesis that microchimerism and HLA genes of host and non-host cells are involved in autoimmune diseases. Alternative sources of microchimerism include transfer from a twin or the mother during pregnancy, or from blood transfusion. Studies of systemic sclerosis, primary biliary cirrhosis, Sjo¨grens syndrome, pruritic eruption of pregnancy, myositis, and thyroid disease have both lent support and raised doubts about a potential role of microchimerism in autoimmune disease. [ABSTRACT FROM AUTHOR]

Abstract: An increase in cervical intraepithelial neoplasia (CIN) has been described in American Indian women in New Mexico. Differences in human leukocyte antigen (HLA) alleles have been reported in cervical intraepithelial neoplasia (CIN) compared with controls in other populations. We investigated HLA alleles and CIN in Southwest American Indian women. The case control study included 89 women with biopsy-proven CIN II/III (diagnosed November 1994 through October 1997) and 271 similar women with normal cervical epithelium from the same clinics. DRB1, DQB1, and DPB1 alleles were determined using DNA typing techniques. DQA1 and HLA-A allele typing was included for some subjects (randomly chosen n = 37 and n = 163 cases and controls, respectively). We found a decreased risk of CIN with DRB1*1402 (OR 0.5, 95% CI 0.3–0.9) and an increased risk with DRB1*1501 (OR 2.7, 95% CI 0.9–7.3). Additionally, DQA1*0102 was associated with increased risk (OR 4.5, 95% CI 1.3–5.3) and HLA-A*02 with decreased risk (OR 0.4, CI 0.2–0.9). Our findings are discussed along with studies in other populations. [Copyright &y& Elsevier]