Ku G, Kronenberg M, Peacock D J, Tempst P, Banquerigo M L, Braun B S, Reeve J R, Brahn E
Department of Medicine, Jonsson Cancer Center, UCLA School of Medicine.
Eur J Immunol. 1993 Mar;23(3):591-9. doi: 10.1002/eji.1830230302.
Collagen arthritis is induced in inbred rats with the injection of native type II collagen. The pathogenesis of this experimental autoimmune disease is T cell dependent. This study demonstrates that collagen-specific T cells, derived from pathogenic and nonpathogenic rat T cell lines, both recognize the same peptide epitope. The epitope, consisting of amino acids 58-73 of cyanogen bromide fragment 11 of type II collagen, was as effective as whole collagen in stimulating a panel of collagen-specific rat/mouse T cell hybridomas. This peptide may, therefore, constitute a dominant epitope for CD4+ rat T cells in their response to type II collagen. Administration of the peptide to either neonatal or adult rats prevented the subsequent induction of experimental arthritis with whole collagen, demonstrating that the in vivo response to this dominant epitope is, therefore, relevant in the pathogenesis of arthritis. Despite its ability to prevent collagen-induced arthritis, administration of this peptide in incomplete Freund's adjuvant intradermally did not induce disease.
通过注射天然II型胶原在近交系大鼠中诱导胶原性关节炎。这种实验性自身免疫性疾病的发病机制依赖于T细胞。本研究表明，源自致病性和非致病性大鼠T细胞系的胶原特异性T细胞都识别相同的肽表位。该表位由II型胶原溴化氰片段11的氨基酸58 - 73组成，在刺激一组胶原特异性大鼠/小鼠T细胞杂交瘤方面与完整胶原同样有效。因此，该肽可能构成CD4 +大鼠T细胞对II型胶原反应中的主要表位。给新生或成年大鼠施用该肽可预防随后用完整胶原诱导的实验性关节炎，表明对该主要表位的体内反应与关节炎的发病机制相关。尽管该肽有预防胶原诱导性关节炎的能力，但在不完全弗氏佐剂中皮内注射该肽并不会诱发疾病。
