Evidence for reduced Th1 function in normal pregnancy: a hypothesis for the remission of rheumatoid arthritis.

Abstract

The mechanisms underlying the pregnancy induced remission of rheumatoid arthritis (RA) remain unclear. We assessed the hypothesis that it reflects systemic physiologic changes in immune response during gestation. We used in vitro whole blood culture systems stimulated with either lipopolysaccharide or phytohemagglutinin to assess cytokine secretion of cells from healthy pregnant and control donors. Interleukin 2 (IL-2) production was decreased during pregnancy, more so in the 3rd trimester, and soluble tumor necrosis factor (TNF) receptor p55 and p75 was increased, again most significantly in the 3rd trimester. TNF-alpha and IL-1 beta were unchanged. These findings are consistent with the hypothesized downregulation of Th1 responses during pregnancy. Further studies to assess the relationship with fetal/maternal HLA class II disparity, and eventually the presence or absence of remission in actual patients with RA, are required.