Mannie M D, Walker M R
Department of Microbiology and Immunology, East Carolina University School of Medicine, Greenville, NC 27858-4354, USA.
J Leukoc Biol. 2001 Aug;70(2):252-60.
Like many T cells in the myelin basic protein (MBP)-specific T-cell repertoire, CD4(-) GP2.3H3.16 (3H3) T cells recognize guinea pig MBP as an agonist but recognize autologous rat (R)MBP as a mixed agonist/antagonist. 3H3 T cells do not exhibit proliferative responses to RMBP but nonetheless respond to RMBP by accumulation of T-cell surface I-A/peptide complexes and generation of T-cell antigen-presenting cell (T-APC) activity. This study showed that presentation of RMBP by 3H3 T-APC is long-lived but is lost during interactions with cognate responders or on overt activation of T-APCs. Presentation of RMBP to encephalitogenic T cells resulted in the reciprocal activation of 3H3 T-APCs as evidenced by blastogenesis, proliferation, and induction of interleukin-2R and OX40 markers on 3H3 T-APC. These data indicate that T-APCs, like B-cell APCs, undergo clonal expansion after presentation of a cognate antigen to T-cell responders.
与髓鞘碱性蛋白(MBP)特异性T细胞库中的许多T细胞一样,CD4(-) GP2.3H3.16(3H3)T细胞将豚鼠MBP识别为激动剂,但将自体大鼠(R)MBP识别为混合激动剂/拮抗剂。3H3 T细胞对R-MBP不表现出增殖反应,但仍通过T细胞表面I-A/肽复合物的积累和T细胞抗原呈递细胞(T-APC)活性的产生对R-MBP作出反应。本研究表明,3H3 T-APC对R-MBP的呈递是长期存在的,但在与同源应答者相互作用期间或T-APC明显激活时会丧失。将R-MBP呈递给致脑炎性T细胞导致3H3 T-APC的相互激活,这通过3H3 T-APC上的芽生、增殖以及白细胞介素-2R和OX40标志物的诱导得以证明。这些数据表明,T-APC与B细胞APC一样,在将同源抗原呈递给T细胞应答者后会发生克隆扩增。