Immunogenetic and serological investigations in nonpregnant and in pregnant women with a history of recurrent spontaneous abortions

Sphingolipid Pathway Regulates Innate Immune Responses at the Fetomaternal Interface during Pregnancy

“…Indeed, TNF-␣ and IFN-␥ have been reported to inhibit fetal development (46,47). In addition, circulating levels of TNF-␣ and IFN-␥ were higher in patients with a subsequent abortion compared with those with normal pregnancy (48,49). In this study, we found that proinflammatory chemokines, CXCL1 and CXCL2, were profoundly increased in the decidua surrounding developing embryos in pregnant Sphk1 Ϫ/Ϫ Sphk2 ϩ/Ϫ female mice.…”

The Power of Observation

“…4 A proclivity to excessive production of TNF-a in vitro is a marker for elevated TNF-a (and elevated Th1 ⁄ Th2 ratios) in vivo, and one of the effects of increased TNF-a can be reduction in Treg cell activity. [4][5][6][7] In the Winger et al's paper, the treatment effect was a combination of improving the implantation rate and reducing post-implantation losses. [4][5][6][7] In the Winger et al's paper, the treatment effect was a combination of improving the implantation rate and reducing post-implantation losses.…”

REVIEW ARTICLE: Cytokine Gene Polymorphisms in Recurrent Spontaneous Abortions: A Comprehensive Review

“…41,42 However, higher circulating levels of TNF-a are associated with subsequent miscarriages, suggesting that this cytokine may be an etiologic factor for RSA. 47,48 Functional polymorphisms at position )308 and )863 in the promoter region of the human TNF-a gene have been reported to be associated with altered TNF-a promoter activity 44,49 and different plasma levels of TNF-a. 45 In women with RSA and multiple implantation failures, absolute cell counts of TNF-a expressing CD3 + ⁄ CD4 + cells were significantly higher than those of non-pregnant fertile women (P < 0.05, P < 0.005 each).…”