Hansen A B, Andersen C B
Department of Pathology, Herlev Hospital, University of Copenhagen, Denmark.
Urol Res. 1994;22(5):309-15. doi: 10.1007/BF00297201.
We examined the role of intercellular adhesion molecule-1 (ICAM-1) and lymphocyte function-associated antigen-1 (LFA-1) during the activation of peripheral blood mononuclear cells (PBMCs) by the human renal carcinoma cell line CaKi-1. ICAM-1 antigen expression was induced on CaKi-1 cells by incubation with either phorbol-12-myristate 13 acetate (PMA) or interferon-gamma (IFN-gamma). Following a thorough washout of PMA and IFN-gamma and subsequent paraformaldehyde fixation, CaKi-1 cell monolayers were cocultered with allogenic PBMCs. While PMA-treated CaKi-1 cells induced PBMC proliferation and interleukin-2 receptor antigen expression, this was not the case for control or IFN-gamma-treated CaKi-1 cells. Furthermore, the induced PBMC proliferation was inhibited by specific monoclonal antibodies against ICAM-1 and LFA-1. Finally, although PMA induced human leukocyte antigen (HL)-A, B, C antigen expression on CaKi-1 cells, a monoclonal antibody against this antigen did not inhibit PBMC proliferation. We conclude that PMA can modulate CaKi-1 cells to stimulate allogenic PBMC proliferation in an ICAM-1/LFA-1 dependent, but HLA-A, B, C-independent, fashion. This stimulation might reside in the long-term activation of protein kinase C, induced by PMA.
我们研究了细胞间黏附分子-1（ICAM-1）和淋巴细胞功能相关抗原-1（LFA-1）在人肾癌细胞系CaKi-1激活外周血单个核细胞（PBMCs）过程中的作用。用佛波醇-12-肉豆蔻酸酯13-乙酸酯（PMA）或干扰素-γ（IFN-γ）孵育可诱导CaKi-1细胞表达ICAM-1抗原。彻底洗脱PMA和IFN-γ并随后用多聚甲醛固定后，将CaKi-1细胞单层与同种异体PBMCs共培养。虽然经PMA处理的CaKi-1细胞可诱导PBMC增殖和白细胞介素-2受体抗原表达，但对照或经IFN-γ处理的CaKi-1细胞则不然。此外，针对ICAM-1和LFA-1的特异性单克隆抗体可抑制诱导的PBMC增殖。最后，虽然PMA可诱导CaKi-1细胞表达人白细胞抗原（HLA）-A、B、C抗原，但针对该抗原的单克隆抗体并不抑制PBMC增殖。我们得出结论，PMA可调节CaKi-1细胞，以ICAM-1/LFA-1依赖但HLA-A、B、C非依赖的方式刺激同种异体PBMC增殖。这种刺激可能源于PMA诱导的蛋白激酶C的长期激活。
