Zamvil S S, Mitchell D J, Moore A C, Schwarz A J, Stiefel W, Nelson P A, Rothbard J B, Steinman L
J Immunol. 1987 Aug 15;139(4):1075-9.
The role of class II restriction in T cell recognition of an epitope of the autoantigen myelin basic protein (MBP) has been investigated. Encephalitogenic PL/J(H-2u) and (PL/J X SJL/J(H-2s))F1 ((PLSJ)F1) clones, isolated after immunization with intact MBP, recognize the N-terminal 11 amino acid residues of MBP in association with I-Au class II molecules. The synthetic peptide MBP 1-11 has been tested in vivo for induction of EAE. Clinical and histological EAE occurs in PL/J and (PLSJ)F1 mice but not SJL/J. The class II restriction of T cells primed with MBP 1-11 has been examined in primary cultures in vitro. Similar to encephalitogenic T cell clones, isolated after continuous selection in vitro, the population of MBP 1-11-specific proliferative PL/J and (PLSJ)F1 T cells, recognize this epitope in association with I-Au class II molecules. Not all MBP-specific T cell clones which are restricted to I-Au class II molecules cause autoimmune encephalomyelitis. The specificity of these non-encephalitogenic clones has been examined in this report. These clones also recognize MBP 1-11. Thus recognition of an encephalitogenic T cell epitope is not sufficient for induction of EAE.
已经研究了II类限制性在T细胞识别自身抗原髓鞘碱性蛋白(MBP)表位中的作用。在用完整MBP免疫后分离出的致脑炎性PL/J(H-2u)和(PL/J×SJL/J(H-2s))F1((PLSJ)F1)克隆,识别与I-Au II类分子相关联的MBP的N端11个氨基酸残基。已在体内测试了合成肽MBP 1-11诱导实验性自身免疫性脑脊髓炎(EAE)的能力。临床和组织学上的EAE出现在PL/J和(PLSJ)F1小鼠中,但不出现在SJL/J小鼠中。已在体外原代培养中检测了用MBP 1-11致敏的T细胞的II类限制性。与在体外连续选择后分离出的致脑炎性T细胞克隆相似,MBP 1-11特异性增殖性PL/J和(PLSJ)F1 T细胞群体识别与I-Au II类分子相关联的该表位。并非所有受I-Au II类分子限制的MBP特异性T细胞克隆都会引起自身免疫性脑脊髓炎。本报告中检测了这些非致脑炎性克隆的特异性。这些克隆也识别MBP 1-11。因此,识别一个致脑炎性T细胞表位不足以诱导EAE。