• 四川大學(xué)華西醫(yī)院（成都，610041）1 風(fēng)濕免疫科，2生物治療國(guó)家重點(diǎn)實(shí)驗(yàn)室;

目的 　研究活動(dòng)期多發(fā)性肌炎患者外周血白細(xì)胞細(xì)胞因子信號(hào)轉(zhuǎn)導(dǎo)蛋白抑制因子（SOCS）1、SOCS2、SOCS3和細(xì)胞因子誘導(dǎo)的含SH2區(qū)域蛋白1（CIS）與正常人表達(dá)的差異，探討SOCS在多發(fā)性肌炎發(fā)病中可能的作用。 方法 　2011年6月－12月，采用實(shí)時(shí)熒光定量聚合酶鏈反應(yīng)法檢測(cè)了14例活動(dòng)期多發(fā)性肌炎患者和14例正常人外周血白細(xì)胞中SOCS1、SOCS2、SOCS3和CIS1基因的相對(duì)表達(dá)量。 結(jié)果 　與對(duì)照組相比，多發(fā)性肌炎癥患者外周血白細(xì)胞基因SOCS 1～3表達(dá)明顯降低（P值均＜0.05），CIS1基因的表達(dá)較對(duì)照組明顯升高（P＜0.05），差異有統(tǒng)計(jì)學(xué)意義。 結(jié)論 　SOCS基因家族可能參與了多發(fā)性肌炎的發(fā)病，該蛋白分子家族的成員可能會(huì)成為多發(fā)性肌炎治療的一種新的候選基因。

引用本文： 孫月池,鄧林,孫文翠,吳永強(qiáng),石桂秀. 多發(fā)性肌炎外周血白細(xì)胞中細(xì)胞因子信號(hào)轉(zhuǎn)導(dǎo)蛋白抑制因子基因表達(dá)的初步研究. 華西醫(yī)學(xué), 2012, 27(4): 481-484. doi: 復(fù)制

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. 　Starr R, Willson TA, Viney EM, et al. A family of cytokine-inducible inhibitors of signalling[J]. Nature, 1997, 387(6636): 917-921.
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. 　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. 　Alexander WS. Suppressors of cytokine signalling (SOCS) in the immune system[J]. Nat Rev Immunol, 2002, 2(6): 410-416.
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. 　Kubo M, Hanada T, Yoshimura A. Suppressors of cytokine signaling and immunity[J]. Nat Immunol, 2003, 4(12): 1169-1176.
8. 　Bohan A, Peter JB.Polymyositis and dermatomyositis (second of two parts) [J]. N Engl J Med, 1975, 292(8): 403-407.
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, Alanärä 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.
15. 　李蘇芬, 方敬愛, 孫艷艷, 等. 阿托伐他汀對(duì)糖尿病腎病大鼠腎組織中JAK/STAT信號(hào)通路及其抑制因子SOCS-1表達(dá)的影響[J]. 中國(guó)中西醫(yī)結(jié)合腎病雜志, 2011, 12(9): 765-768.
16. 　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.
  1. 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. 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. 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. 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. 13. 　Isomaki P, Alanärä T, Isohanni P, et al. The expression of SOCS is altered in rheumatoid arthritis[J]. Rheumatology (Oxford), 2007, 46(10): 1538-1546.
  14. 14. 　Walker JG, Smith MD. The Jak-STAT pathway in rheumatoid arthritis[J]. J Rheumatol, 2005, 32(9): 1650-1653.
  15. 15. 　李蘇芬, 方敬愛, 孫艷艷, 等. 阿托伐他汀對(duì)糖尿病腎病大鼠腎組織中JAK/STAT信號(hào)通路及其抑制因子SOCS-1表達(dá)的影響[J]. 中國(guó)中西醫(yī)結(jié)合腎病雜志, 2011, 12(9): 765-768.
  16. 16. 　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. 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. 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. 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.