PT  - JOURNAL ARTICLE
AU  - Suzuki, T
AU  - Hiromatsu, K
AU  - Ando, Y
AU  - Okamoto, T
AU  - Tomoda, Y
AU  - Yoshikai, Y
TI  - Regulatory role of gamma delta T cells in uterine intraepithelial lymphocytes in maternal antifetal immune response.
DP  - 1995 May 01
TA  - The Journal of Immunology
PG  - 4476--4484
VI  - 154
IP  - 9
4099  - http://www.jimmunol.org/content/154/9/4476.short
4100  - http://www.jimmunol.org/content/154/9/4476.full
SO  - J. Immunol.1995 May 01; 154
AB  - To elucidate the potential roles of the gamma delta T cells in uterine intraepithelial lymphocytes (IEL) in the regulation of maternal antifetal immune response during pregnancy, we examined the kinetics and function of gamma delta T cells in uterine IEL obtained from (C3H/He x AKR/J) pregnancy. The number of gamma delta T cells increased in the uterine IEL in (C3H/HexAKR/J) pregnancy more than those in (C3H/HexC3H/He) pregnancy and much more than in nonpregnant C3H/He mice. The uterine IEL in (C3H/HexC3H/He) pregnancy significantly proliferated in response to AKR/J stimulator cells. In contrast, the uterine IEL in (C3H/HexAKR/J) pregnancy showed little, if any, proliferation in response to the same stimulator cells. gamma delta T cell depletion from the uterine IEL in (C3H/HexAKR/J) pregnancy restored their responsiveness against AKR/J stimulator cells. Both gamma delta T cell-enriched fraction and alpha beta T cell-depleted fraction, but neither gamma delta T cell-depleted fraction nor alpha beta T cell-enriched fraction in the uterine IEL exhibited suppressive activity against allogeneic responses of nonpregnant C3H/He LN cells. This suppressive activity was shown by transferring the supernatant of culture medium in the uterine IEL stimulated with AKR/J cells that contained a large amount of TGF-beta, and the suppressive activity was significantly blocked by addition of anti-TGF-beta mAb to the culture. Taken together, our results suggest that gamma delta T cells in the uterine IEL suppress the maternal antifetal immune response at the maternal-fetal interface at least in part through TGF-beta production to prevent a rejection of the fetus.