Dang Y, Heyborne K D
Reproductive Immunology Laboratory, Swedish Medical Center, Denver CO 80110, USA.
J Immunol. 2001 Mar 15;166(6):3641-4. doi: 10.4049/jimmunol.166.6.3641.
The peri-implantation uterus contains an expanded population of NK1.1(+) V alpha 14(+) TCR(int) (NKT) lymphocytes. Although these cells bear the above features in common with other NKT cells populations in thymus, bone marrow, liver, and spleen, they differ from these other populations in terms of an altered V beta repertoire and absence of a CD4(+) component. In this study, we demonstrate that the uterine population also differs from other NKT cell populations because they recognize a class I/class I-like molecule other than CD1, whereas most previously described V alpha 14(+) NKT cells are CD1-restricted. Moreover, the class I/class I-like molecule leading to the uterine NKT cell expansion may be supplied by the fetus. These data demonstrate a novel mechanism whereby the fetus is capable of modulating the maternal immune system.
植入前子宫中含有大量扩增的NK1.1(+)Vα14(+)TCR(int)(NKT)淋巴细胞。尽管这些细胞与胸腺、骨髓、肝脏和脾脏中的其他NKT细胞群体具有上述共同特征,但它们在Vβ库改变和缺乏CD4(+)成分方面与其他群体不同。在本研究中,我们证明子宫中的NKT细胞群体也与其他NKT细胞群体不同,因为它们识别的是除CD1之外的I类/I类样分子,而大多数先前描述的Vα14(+)NKT细胞是受CD1限制的。此外,导致子宫NKT细胞扩增的I类/I类样分子可能由胎儿提供。这些数据证明了一种新的机制,即胎儿能够调节母体免疫系统。