Huang K, Beigi M, Daynes R A
Department of Pathology, University of Utah Medical Center, Salt Lake City 84132.
Reg Immunol. 1990 Mar-Apr;3(2):103-11.
The MEL-14 receptor (MEL-14 R) expressed by murine lymphocytes represents the peripheral lymph node-specific homing receptor, and is essential for murine lymphocytes to specifically adhere to high endothelial venules (HEV) of the peripheral lymph nodes and to ultimately migrate in vivo into the parenchyma of this lymphoid organ. A Peyer's patch-specific homing receptor, termed LPAM, is now appreciated to mediate murine lymphocyte adhesion to Peyer's patch HEV. We previously demonstrated that the cell surface density of the MEL-14 R was markedly reduced following PMA-induced protein kinase C activation of lymphocytes. In the present study, we investigated the phenotypic and functional expression of LPAM by murine lymphocytes exposed to PMA. The results show that the surface expression of LPAM on activated lymphocytes remains constant under conditions where MEL-14 R is downregulated significantly. Additionally, the surface expression of LPAM is not influenced by calcium ionophore, either alone or in combination with PMA, whereas the PMA-induced loss of MEL-14 R is synergized by calcium ionophore. Therefore, LPAM and MEL-14 R expression are differentially regulated by activated murine lymphocytes. LPAM expressed by TK1 (Peyer's patch HEV-binding murine lymphoma) and MEL-14 R expressed by 38C13 (peripheral lymph node HEV-binding murine lymphoma) were found to be regulated by the consequences of PMA activation in a pattern similar to that of normal lymphocytes. Furthermore, we provide evidence that MEL-14 R internalization is not involved in the loss of the receptor expressed by activated lymphocytes.(ABSTRACT TRUNCATED AT 250 WORDS)
小鼠淋巴细胞表达的MEL-14受体(MEL-14 R)代表外周淋巴结特异性归巢受体,对于小鼠淋巴细胞特异性黏附于外周淋巴结的高内皮微静脉(HEV)并最终在体内迁移至该淋巴器官实质至关重要。一种称为LPAM的派伊尔结特异性归巢受体,现已知介导小鼠淋巴细胞与派伊尔结HEV的黏附。我们先前证明,淋巴细胞经佛波酯(PMA)诱导蛋白激酶C激活后,MEL-14 R的细胞表面密度显著降低。在本研究中,我们调查了经PMA处理的小鼠淋巴细胞中LPAM的表型和功能表达。结果显示,在MEL-14 R显著下调的条件下,活化淋巴细胞上LPAM的表面表达保持恒定。此外,LPAM的表面表达不受钙离子载体单独或与PMA联合作用的影响,而钙离子载体可协同PMA诱导的MEL-14 R丢失。因此,活化的小鼠淋巴细胞对LPAM和MEL-14 R的表达调控存在差异。发现TK1(与派伊尔结HEV结合的小鼠淋巴瘤)表达的LPAM和38C13(与外周淋巴结HEV结合的小鼠淋巴瘤)表达的MEL-14 R受PMA激活的影响,其调控模式与正常淋巴细胞相似。此外,我们提供证据表明,MEL-14 R的内化与活化淋巴细胞表达的该受体丢失无关。(摘要截短于250词)