Englert M E, Landes M J, Oronsky A L, Kerwar S S
Cell Immunol. 1984 Sep;87(2):357-65. doi: 10.1016/0008-8749(84)90005-4.
Intravenous administration of Type II collagen to rats prior to immunization with Type II collagen suppresses hind paw inflammation, humoral response to Type II collagen, and the severity of the arthritic lesion. Suppression of inflammation and its severity as well as the humoral response can also be induced by the prior intravenous administration of alpha 1 (II) CB10 a cyanogen bromide peptide derived from Type II collagen. Suppression of arthritis is disease specific; intravenous administration of either Type II collagen or alpha 1 (II) CB10 does not have an effect on adjuvant-induced arthritis. These studies indicate that structural determinants of alpha 1 (II) CB10 (Mr 30,000), a peptide located near the carboxy terminus of the collagen molecule, can induce suppression and suggest that these determinants may be responsible for the suppression of arthritis when Type II collagen is administered intravenously.
在用II型胶原蛋白免疫大鼠之前,静脉注射II型胶原蛋白可抑制后爪炎症、对II型胶原蛋白的体液反应以及关节炎病变的严重程度。通过预先静脉注射α1(II)CB10(一种源自II型胶原蛋白的溴化氰肽),也可诱导炎症及其严重程度以及体液反应的抑制。关节炎的抑制具有疾病特异性;静脉注射II型胶原蛋白或α1(II)CB10对佐剂诱导的关节炎均无影响。这些研究表明,位于胶原蛋白分子羧基末端附近的肽α1(II)CB10(分子量30,000)的结构决定簇可诱导抑制作用,并表明当静脉注射II型胶原蛋白时,这些决定簇可能是抑制关节炎的原因。