Journal
SCIENTIFIC REPORTS
Volume 6, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/srep36560
Keywords
-
Categories
Funding
- National Basic Research Program of China [2013CB967404]
- National Natural Science Foundation of China [81501333, 81125004, 31171439, 31671567]
- Natural Science Foundation of Hubei Province [2015CFB722]
- Fund for Outstanding Academic Leaders in Shanghai, China [12XD1406600, 2013-049]
- Shanghai Municipal Health Bureau [20154Y0068]
- Shanghai Municipal Commission of Health and Family Planning Program [15GWZK0701]
Ask authors/readers for more resources
A deeper understanding of the immunological events during pregnancy will provide novel insights into the pathogenesis of pregnancy complications. The fundamental function of T follicular helper (Tfh) cells is to provide cognate help to B cells. Dysregulations of Tfh-cell function and/or development can result in various immunological diseases. However, the role and characteristics of Tfh cells during pregnancy remain unknown. Herein, an allogeneic-normal-pregnant mouse model was used, and we found that the CD4(+) T cells residing at the uterus and placenta (UP) displayed a Tfh-like phenotype; and the UP-derived CD4(+) CXCR5(hi)PD-1(hi) and CD4(+) CXCR5(hi)ICOS(hi) Tfh cells, which showed a memory/activation phenotype, reached their peak at mid-pregnancy. These Tfh cells were located abundantly in the uterus at mid-pregnancy, but greatly increased in the placenta at late-pregnancy. Furthermore, increased foetal resorption by PDL1 blockade correlated with enhanced accumulation of Tfh cells and upregulated expressions of ICOS and PD-1 on these cells. Collectively, our findings are the first to indicate that an adequate and balanced accumulation of Tfh cells during gestation is likely to help maintaining a successful pregnancy, whereas an excessively high level of these cells could lead to abortion.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available