Ruiz P J, Garren H, Hirschberg D L, Langer-Gould A M, Levite M, Karpuj M V, Southwood S, Sette A, Conlon P, Steinman L
Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305, USA.
J Exp Med. 1999 Apr 19;189(8):1275-84. doi: 10.1084/jem.189.8.1275.
Molecular mimicry refers to structural homologies between a self-protein and a microbial protein. A major epitope of myelin basic protein (MBP), p87-99 (VHFFKNIVTPRTP), induces experimental autoimmune encephalomyelitis (EAE). VHFFK contains the major residues for binding of this self-molecule to T cell receptor (TCR) and to the major histocompatibility complex. Peptides from papilloma virus strains containing the motif VHFFK induce EAE. A peptide from human papilloma virus type 40 (HPV 40) containing VHFFR, and one from HPV 32 containing VHFFH, prevented EAE. A sequence from Bacillus subtilis (RKVVTDFFKNIPQRI) also prevented EAE. T cell lines, producing IL-4 and specific for these microbial peptides, suppressed EAE. Thus, microbial peptides, differing from the core motif of the self-antigen, MBPp87-99, function as altered peptide ligands, and behave as TCR antagonists, in the modulation of autoimmune disease.
分子模拟是指自身蛋白与微生物蛋白之间的结构同源性。髓鞘碱性蛋白（MBP）的一个主要表位，即p87 - 99（VHFFKNIVTPRTP），可诱发实验性自身免疫性脑脊髓炎（EAE）。VHFFK包含该自身分子与T细胞受体（TCR）以及主要组织相容性复合体结合的主要残基。来自含有基序VHFFK的乳头瘤病毒株的肽可诱发EAE。来自人乳头瘤病毒40型（HPV 40）的含VHFFR的肽以及来自HPV 32的含VHFFH的肽可预防EAE。来自枯草芽孢杆菌的一个序列（RKVVTDFFKNIPQRI）也可预防EAE。产生白细胞介素4且对这些微生物肽具有特异性的T细胞系可抑制EAE。因此，与自身抗原MBPp87 - 99的核心基序不同的微生物肽，在自身免疫性疾病的调节中作为改变的肽配体发挥作用，并表现为TCR拮抗剂。
Zotero 插件
