Hudrisier Denis, Bongrand Pierre
INSERM U 395, CHU Purpan and Paul Sabatier University, BP3028 31024 Toulouse Cedex 3, France.
FASEB J. 2002 Apr;16(6):477-86. doi: 10.1096/fj.01-0933rev.
Upon physiological stimulation, receptors with tyrosine kinase activity (RTK) are rapidly internalized together with their soluble ligands. T cell activation is the consequence of recognition by the T cell receptor (TCR) of specific peptide-major histocompatibility protein complexes (peptide-MHC) present at the membrane of antigen-presenting cells (APC). The TCR belongs to the RTK family and is known to be endocytosed upon ligand recognition. It differs from most other RTK in that its ligand, the peptide-MHC complex, is membrane bound and the TCR-ligand interaction is quite weak. Recent experiments have shown that the TCR ligand becomes internalized by T cells upon stimulation. Here we review current knowledge on the molecular mechanisms by which the membrane-bound MHC molecules can be transferred onto T cells, and propose hypotheses on the role this phenomenon could play in physio-pathological situations involving T cells.
在生理刺激下,具有酪氨酸激酶活性的受体(RTK)会与其可溶性配体一起迅速内化。T细胞活化是T细胞受体(TCR)识别抗原呈递细胞(APC)膜上存在的特异性肽 - 主要组织相容性蛋白复合物(肽 - MHC)的结果。TCR属于RTK家族,已知在配体识别后会被内吞。它与大多数其他RTK的不同之处在于其配体,即肽 - MHC复合物,是膜结合的,并且TCR - 配体相互作用相当弱。最近的实验表明,TCR配体在刺激后会被T细胞内化。在这里,我们综述了关于膜结合的MHC分子转移到T细胞上的分子机制的现有知识,并对这一现象在涉及T细胞的生理病理情况下可能发挥的作用提出假设。