目的 檢測系統(tǒng)性紅斑狼瘡（SLE）患者CD4+CD25+調(diào)節(jié)性T細(xì)胞（Treg）上Ⅰ型干擾素受體（IFNAR）的分布格局，了解Ⅰ型干擾素對SLE患者CD4+CD25+Treg產(chǎn)生直接影響的作用靶點(diǎn)。 方法 選取2010年9月－2011年10月間20例初次確診的SLE患者（SLE組）和20例健康女性（對照組），分離SLE患者和對照組的外周血單個核細(xì)胞，采用流式細(xì)胞術(shù)測定CD4+CD25+Treg上IFNAR的表達(dá)。 結(jié)果 ?、?IFNAR1、IFNAR2在Treg和CD4+CD25? T細(xì)胞表面均有表達(dá)；兩組Treg表面IFNAR1和IFNAR2的表達(dá)水平均高于CD4+CD25? T細(xì)胞。② 與對照組相比，SLE組Treg表面IFNAR1表達(dá)的平均熒光強(qiáng)度明顯增高（P=0.001）。③ SLE組Treg表面IFNAR1表達(dá)平均熒光強(qiáng)度與疾病活動指數(shù)評分呈正相關(guān)（rs=0.505，P=0.023）。 結(jié)論 SLE患者CD4+CD25+Treg表面相對高表達(dá)IFNAR1且與疾病活動性相關(guān)，提示Ⅰ型干擾素以Treg上IFNAR為靶點(diǎn)在SLE發(fā)病機(jī)制中可能發(fā)揮重要作用，為SLE等自身免疫性疾病治療尋找新的干預(yù)手段提供了理論基礎(chǔ)。
引用本文： 孫文翠,嚴(yán)冰,石桂秀,何燕,孫月池. Ⅰ型干擾素受體在系統(tǒng)性紅斑狼瘡患者CD4+CD25+調(diào)節(jié)性T細(xì)胞的檢測和意義. 華西醫(yī)學(xué), 2012, 27(6): 823-827. doi: 復(fù)制
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- 1. Chen Y, Cuda C, Morel L. Genetic determination of T cell help in loss of tolerance to nuclear antigens[J]. J Immunol, 2005, 174(12): 7692-7702.
- 2. Yan B, Ye S, Chen G, et al. Dysfunctional CD4+, CD25+ regulatory T cells in untreated active systemic lupus erythematosus secondary to interferon-alpha-producing antigen-presenting cells[J]. Arthritis Rheum, 2008, 58(3): 801-812.
- 3. Banchereau J, Pascual V. TypeⅠinterferon in systemic lupus erythematosus and other autoimmune diseases[J]. Immunity, 2006, 25(3): 383-392.
- 4. Blanco P, Palucka AK, Gill M, et al. Induction of dendritic cell differentiation by IFN-alpha in systemic lupus erythematosus[J]. Science, 2001, 294(5546): 1540-1543.
- 5. Santiago-Raber ML, Baccala R, Haraldsson KM, et al. Type-Ⅰinterferon receptor deficiency reduces lupus-like disease in NZB mice[J]. J Exp Med, 2003, 197(6): 777-788.
- 6. Nacionales DC, Kelly-Scumpia KM, Lee PY, et al. Deficiency of the typeⅠinterferon receptor protects mice from experimental lupus[J]. Arthritis Rheum, 2007, 56(11): 3770-3783.
- 7. Foster GR, Masri SH, David R, et al. IFN-α subtypes differentially affect human T cell motility[J]. J Immunol, 2004, 173(3): 1663-1670.
- 8. Pascual V, Farkas L, Banchereau J. Systemic lupus erythematosus: all roads lead to typeⅠinterferons[J]. Curr Opin Immunol, 2006, 18(6): 676-682.
- 9. Ronnblom L, Eloranta ML, Alm GV. The typeⅠinterferon system in systemic lupus erythematosus[J]. Arthritis Rheum, 2006, 54(2): 408-420.
- 10. Barrat FJ, Meeker T, Gregorio J, et al. Nucleic acids of mammalian origin can act as endogenous ligands for Toll-like receptors and may promote systemic lupus erythematosus[J]. J Exp Med, 2005, 202(8): 1131-1139.
- 11. Savarese E, Chae OW, Trowitzsch S, et al. U1 small nuclear ribonucleoprotein immune complexes induce typeⅠinterferon in plasmacytoid dendritic cells through TLR7[J]. Blood, 2006, 107(8): 3229-3234.
- 12. Vollmer J, Tluk S, Schmitz C, et al. Immune stimulation mediated by autoantigen binding sites within small nuclear RNAs involves Toll-like receptors 7 and 8[J]. J Exp Med, 2005, 202(11): 1575-1585.
- 13. Means TK, Latz E, Hayashi F, et al. Human lupus autoantibody-DNA complexes activate DCs through cooperation of CD32 and TLR9[J]. J Clin Invest, 2005, 115(2): 407-417.