Basu Satarupa, Eriksson Mikael, Pioli Patricia A, Conejo-Garcia Jose, Mselle Teddy F, Yamamoto Satoshi, Wira Charles R, Sentman Charles L
Department of Microbiology & Immunology, Dartmouth Medical School, Lebanon, NH 03756, USA.
Am J Reprod Immunol. 2009 Jan;61(1):52-61. doi: 10.1111/j.1600-0897.2008.00661.x.
The initiation of an immune response often involves the cooperation of various innate immune cells. In the human endometrium, uterine natural killer (uNK) cells and uterine macrophages are present in significant numbers and in close proximity, yet how they cooperatively respond to infectious challenge is poorly understood.
Primary autologous uNK cells and macrophages were co-cultured to determine functional interactions after stimulation with pathogen-associated molecular patterns.
After stimulation by polyI:C, human uNK cells interact with autologous uterine macrophages and produce interferon-gamma in an NKG2D-dependent manner. Stimulated primary uterine macrophages up-regulated the expression of MHC Class I chain-related protein A (MICA), but expression of the cognate receptor NKG2D remained unchanged on uNK cells, even in the presence of cytokines.
This study demonstrates that the NKG2D-MICA interaction is an important molecular mechanism that is involved in the innate immune response to microbial signals in the human uterine endometrium.
免疫反应的启动通常涉及多种天然免疫细胞的协作。在人类子宫内膜中，子宫自然杀伤（uNK）细胞和子宫巨噬细胞数量众多且位置相邻，但它们如何协同应对感染性挑战却鲜为人知。
将原代自体uNK细胞和巨噬细胞共同培养，以确定在用病原体相关分子模式刺激后的功能相互作用。
在用聚肌胞苷酸（polyI:C）刺激后，人类uNK细胞与自体子宫巨噬细胞相互作用，并以NKG2D依赖的方式产生γ干扰素。受刺激的原代子宫巨噬细胞上调了MHC I类链相关蛋白A（MICA）的表达，但即使在存在细胞因子的情况下，uNK细胞上同源受体NKG2D的表达仍保持不变。
本研究表明，NKG2D-MICA相互作用是参与人类子宫内膜对微生物信号天然免疫反应的一种重要分子机制。
