제2형 콜라겐으로 경구관용을 유도한 관절염 모델 마우스의 비장림프구내의 보조자극인자 및 STAT/SOCS 신호전달 인자의 발현 양상조사

• Published in: Immune network Vol. 3; no. 3; pp. 248 - 254
• Main Authors: 이강은(Kang-Eun Lee), 황수연(Sue-Yun Hwang), 민소연(So-Youn Min), 김호연(Ho-Youn Kim)
• Format: Journal Article
• Language: Korean
• Published: 대한면역학회 2003
• Subjects: type II collagen; co-stimulatory molecules; STAT; SOCS; Oral tolerance; rheumatoid arthritis
• ISSN: 1598-2629; 2092-6685

Oral administration of antigen has long been used in the induction of immune tolerance in various animal models of autoimmune diseases including rheumatoid arthritis (RA). Alleveation of arthritogenic symptoms has been reported from RA patients who received oral administration of type II collagen (CII) without side effects, however its rather inconsistent therapeutic efficacy and variation among patients calls for more detailed investigation on the mechanism of oral tolerance to be settled as regular treatment for RA. In an attempt to understand the immunogenic processes underpinning tolerance induction by orally administered CII, we analyzed changes in the expression of costimulatory molecules and STAT/SOCS signaling messengers in the mouse model of collagen induced arthritis (CIA). We found thatin the spleen of CIA mice, that has been undergone repeated oral feeding of CII prior to the induction of arthritis, showed increased promortion of CTLA4 expressing lymphocytes than in the spleen of PBS fed control. On the other hand, cells expressing CD28 or ICOS were decreased in the spleen of tolerized mice. Tolerance induction by oral CII administration also enhanced the expression of STAT6 in both RNA and protein level, while not affecting the expression of STAT3. The expression of SOCS3, which hasbeen known to transmit STAT-mediated signals from Th2 type cytokines, remained unchanged in the spleen of tolerized mice. Interestingly transcript of SOCS1, which has been associated with Th1 related pathways, was only visible in the spleen of tolerized but not of control mice, suggesting that as in the case of IL-6 signaling, it may exert a feed back inhibition toward the Th1 type stimulation.