Iwata M, Yagihashi A, Roat M I, Zeevi A, Iwaki Y, Thoft R A
Department of Ophthalmology, University of Pittsburgh School of Medicine, Pennsylvania.
Invest Ophthalmol Vis Sci. 1994 Nov;35(12):3991-4000.
To achieve a better understanding of the mechanism of corneal immune diseases, including corneal allograft rejection, the authors examined the potential of human corneal epithelial (HCE) cells to activate allogeneic T lymphocytes.
The mixed lymphocyte-HCE cell reaction (MLCER) was performed as follows: HCE cells from primary cultures, with or without treatment with interferon-gamma (IFN-gamma), were treated with mitomycin C and then mixed with peripheral blood lymphocytes (PBL) from normal volunteers. Triplicate cultures were incubated for 7 days. Interleukin-1-alpha (IL-1-alpha) was added to some cultures to examine its effect on MLCER: The lymphocyte responses were measured by 3H-thymidine uptake for the last 18 hours of incubation in MLCER:
IFN-gamma-treated, HLA-class-II-bearing HCE cells stimulated allogenic lymphocytes, whereas IFN-gamma nontreated, class-II-negative HCE cells did not. The stimulation by IFN-gamma-treated HCE cells was blocked by anti-HLA class II monoclonal antibody. In addition, exogenous IL-1-alpha reduced the lymphocyte response in MLCER: This effort was inhibited by indomethacin.
This study demonstrates that HLA-class-II-bearing HCE cells can activate allogeneic PBL by a major histocompatibility complex class II-dependent mechanism. In addition, HCE cells may regulate immune reactions, probably through prostaglandin production caused by IL-1.
为了更好地理解角膜免疫疾病的机制，包括角膜移植排斥反应，作者研究了人角膜上皮（HCE）细胞激活同种异体T淋巴细胞的潜力。
混合淋巴细胞 - HCE细胞反应（MLCER）按以下方式进行：来自原代培养的HCE细胞，无论是否用γ干扰素（IFN-γ）处理，先用丝裂霉素C处理，然后与正常志愿者的外周血淋巴细胞（PBL）混合。一式三份的培养物孵育7天。将白细胞介素-1-α（IL-1-α）添加到一些培养物中以检查其对MLCER的影响：在MLCER孵育的最后18小时通过3H-胸腺嘧啶核苷摄取测量淋巴细胞反应。
经IFN-γ处理、携带HLA-II类分子的HCE细胞刺激同种异体淋巴细胞，而未经IFN-γ处理、II类阴性的HCE细胞则不能。经IFN-γ处理的HCE细胞的刺激被抗HLA II类单克隆抗体阻断。此外，外源性IL-1-α降低了MLCER中的淋巴细胞反应：这种作用被吲哚美辛抑制。
本研究表明，携带HLA-II类分子的HCE细胞可通过主要组织相容性复合体II类依赖性机制激活同种异体PBL。此外，HCE细胞可能通过IL-1引起的前列腺素产生来调节免疫反应。
