[ 1 ] Lundberg IE. New possibilities to achieve increased understanding of disease mechanisms in idiopathic inflammatory myopathies[J]. Curr Opin Rheumatol, 2002, 14(6): 639-642.
[2]
[ 2 ] Starr R, Willson TA, Viney EM, et al. A family of cytokine-inducible inhibitors of signalling[J]. Nature, 1997, 387(6636): 917-921.
[3]
[ 3 ] Endo TA, Masuhara M, Yokouchi M, et al. A new protein containing an SH2 domain that inhibits JAK kinases[J]. Nature, 1997, 387(6636): 921-924.
[4]
[ 4 ] Yoshimura A, Nishinakamura H, Matsumura Y, et al. Negative regulation of cytokine signaling and immune responses by SOCS proteins[J]. Arthritis Res Ther, 2005, 7(3): 100-110.
[5]
[ 5 ] Alexander WS. Suppressors of cytokine signalling (SOCS) in the immune system[J]. Nat Rev Immunol, 2002, 2(6): 410-416.
[6]
[ 6 ] Alexander WS, Hilton DJ. The role of suppressors of cytokine signaling (SOCS) proteins in regulation of the immune response[J]. Annu Rev Immunol, 2004, 22: 503-529.
[7]
[ 7 ] Kubo M, Hanada T, Yoshimura A. Suppressors of cytokine signaling and immunity[J]. Nat Immunol, 2003, 4(12): 1169-1176.
[8]
[ 8 ] Bohan A, Peter JB.Polymyositis and dermatomyositis (second of two parts) [J]. N Engl J Med, 1975, 292(8): 403-407.
[9]
[ 9 ] Bohan A, Peter JB. Polymyositis and dermatomyositis (first of two parts) [J]. N Engl J Med, 1975, 292(7): 344-347.
[10]
Miller FW, Rider LG, Chung YL, et al. Proposed preliminary core set measures for disease outcome assessment in adult and juvenile idiopathic inflammatory myopathies[J]. Rheumatology (Oxford), 2001, 40(11): 1262-1273.
[11]
Hanada T, Kinjyo I, Inagaki-Ohara K, et al. Negative regulation of cytokine signaling by CIS/SOCS family proteins and their roles in inflammatory diseases[J]. Rev Physiol Biochem Pharmacol, 2003, 149: 72-86.
[12]
Chan HC, Ke LY, Chang LL, et al. Suppressor of cytokine signaling 1 gene expression and polymorphisms in systemic lupus erythematosus[J]. Lupus, 2010, 19(6): 696-702.
[13]
Isomaki P, Alan?r? T, Isohanni P, et al. The expression of SOCS is altered in rheumatoid arthritis[J]. Rheumatology (Oxford), 2007, 46(10): 1538-1546.
[14]
Walker JG, Smith MD. The Jak-STAT pathway in rheumatoid arthritis[J]. J Rheumatol, 2005, 32(9): 1650-1653.
Veenbergen S, Bennink MB, Affandi AJ, et al. A pivotal role for antigen-presenting cells overexpressing SOCS3 in controlling invariant NKT cell responses during collagen-induced arthritis[J]. Ann Rheum Dis, 2011, 70(12): 2167-2175
[17]
Ramgolam VS, Markovic-Plese S. Regulation of suppressors of cytokine signaling as a therapeutic approach in autoimmune diseases, with an emphasis on multiple sclerosis[J]. J Signal Transduct, 2011, 2011: doi: IO.1155/2011/635721.
[18]
Matsumoto A, Masuhara M, Mitsui K, et al. CIS, a cytokine inducible SH2 protein, is a target of the JAK-STAT5 pathway and modulates STAT5 activation[J]. Blood, 1997, 89(9): 3148-3154.
[19]
Tsao JT, Kuo CC, Lin SC. The analysis of CIS, SOCS1, SOSC2 and SOCS3 transcript levels in peripheral blood mononuclear cells of systemic lupus erythematosus and rheumatoid arthritis patients[J]. Clin Exp Med, 2008, 8(4): 179-185.