T/B淋巴亚群紊乱在类风湿性关节炎患者中的临床意义研究
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摘要
目的探讨类风湿性关节炎(Rheumatoid arthritis, RA)患者与体检健康人外周血T淋巴细胞亚群、B淋巴细胞及自然杀伤(NK)细胞的频率分布及临床意义。方法收集2018年1月-2018年5月在浙江省人民医院住院的50例RA患者和50例健康人的外周血,采用荧光标记抗体和外周血共同孵育的方法,用流式细胞技术检测CD3~+、CD4~+、CD8~+T淋巴细胞亚群、B淋巴细胞、NK细胞的百分比,并把这些淋巴细胞亚群百分比与疾病活动指数DAS28(Disease Activity Score 28)的相关性作统计学分析。结果 50例RA患者的CD3~+、CD4~+T淋巴细胞和B淋巴细胞频率显著高于50例健康人(P<0.05),NK细胞频率显著低于健康人(P<0.05),且CD4~+T淋巴细胞和B淋巴细胞的分布频率与DAS28呈正相关,差异均有统计学意义(P<0.05)。结论 CD4~+T淋巴细胞和B淋巴细胞在RA患者的疾病进展中扮演重要角色。
Objective To investigate the frequency distribution and the clinical significance of T lymphocyte subsets, B cells and natural killer(NK) cells in the peripheral blood of patients with rheumatoid arthritis(RA) and healthy people. Methods The peripheral blood samples of 50 hospitalized RA patients and 50 healthy persons from January to May 2018 in Zhejiang Province People's Hospital were collected, then incubated these blood samples with the fluorescent label antibody. Flow cytometry was used to detect the percentages of CD3~+, CD4~+, CD8~+T lymphocyte subsets, B lymphocyte and NK cells. The correlation between the percentage of lymphocyte subsets and DAS28(Disease Activity Score 28) was also analyzed. Results The CD3~+, CD4~+T lymphocyte and B lymphocyte of 50 patients with RA were significantly higher than that of 50 healthy persons(P<0.05), the frequency of NK cells was significantly lower than that of healthy people(P<0.05), and there was a positive correlation between CD4~+T lymphocyte or B lymphocyte with the DAS28, with the above differences statistically significant(P<0.05). Conclusion CD4~+T lymphocytes and B lymphocytes may play a critical role in the clinical progression of RA patients.
Objective To investigate the frequency distribution and the clinical significance of T lymphocyte subsets, B cells and natural killer(NK) cells in the peripheral blood of patients with rheumatoid arthritis(RA) and healthy people. Methods The peripheral blood samples of 50 hospitalized RA patients and 50 healthy persons from January to May 2018 in Zhejiang Province People's Hospital were collected, then incubated these blood samples with the fluorescent label antibody. Flow cytometry was used to detect the percentages of CD3~+, CD4~+, CD8~+T lymphocyte subsets, B lymphocyte and NK cells. The correlation between the percentage of lymphocyte subsets and DAS28(Disease Activity Score 28) was also analyzed. Results The CD3~+, CD4~+T lymphocyte and B lymphocyte of 50 patients with RA were significantly higher than that of 50 healthy persons(P<0.05), the frequency of NK cells was significantly lower than that of healthy people(P<0.05), and there was a positive correlation between CD4~+T lymphocyte or B lymphocyte with the DAS28, with the above differences statistically significant(P<0.05). Conclusion CD4~+T lymphocytes and B lymphocytes may play a critical role in the clinical progression of RA patients.
引文
[1] Lau CS,Chia F,Harrison A,et al.APLAR rheumatoid arthritis treatment recommendations[J].Int J Rheum Dis,2015,18(7):685-713.
[2] Glant TT,Mikecz K,Rauch TA.Epigenetics in the pathogenesis of rheumatoid arthritis[J].BMC Med,2014,5(12):32-35.
[3] de Pablo P,Dietrich T,Chapple IL,et al.The autoantibody repertoire in periodontitis:a role in the induction of autoimmunity to citrullinated proteins in rheumatoid arthritis[J].Ann Rheum Dis,2014,73(3):580-586.
[4] Angelotti F,Parma A,Cafaro G,et al.One year in review 2017:pathogenesis of rheumatoid arthritis[J].Clin Exp Rheumatol,2017,35(3):368-378.
[5] Hauser B,Harre U.The Role of Autoantibodies in Bone Metabolism and Bone Loss[J].Calcif Tissue Int,2018,102(5):522-532.
[6] McInnes IB,Schett G.Pathogenetic insights from the treatment of rheumatoid arthritis[J].Lancet,2017,389(10086):2328-2337.
[7] Futo G,Somogyi A,Szekanecz Z.Visualization of DAS28,SDAI,and CDAI:the magic carpets of rheumatoid arthritis[J].Clin Rheumatol,2014,33(5):623-629.
[8] Bashford-Rogers RJM,Smith KGC,Thomas DC.Antibody repertoire analysis in polygenic autoimmune diseases[J].Immunology,2018,2(5):51-56
[9] Scherer HU,Huizinga TWJ,Kronke G,et al.The B cell response to citrullinated antigens in the development of rheumatoid arthritis[J].Nat Rev Rheumatol,2018,14(3):157-169.
[10] Wu H,Deng Y,Feng Y,et al.Epigenetic regulation in B-cell maturation and its dysregulation in autoimmunity[J].Cell Mol Immunol,2018,4(6):81-88.
[11] Pala O,Diaz A,Blomberg BB,et al.B Lymphocytes in Rheumatoid Arthritis and the Effects of Anti-TNF-alpha Agents on B Lymphocytes:A Review of the Literature[J].Clin Ther,2018,8(9):1023-1029.
[12] Benoist C,Mathis D.Treg cells,life history,and diversity[J].Cold Spring Harb Perspect Biol,2012,4(9):43-48.
[13] Cooles FA,Isaacs JD,Anderson AE.Treg cells in rheumatoid arthritis:an update[J].Curr Rheumatol Rep,2013,15(9):352-357.
[14] Wing K,Suri-Payer E,Rudin A.CD4+CD25+-regulatory T cells from mouse to man[J].Scand J Immunol,2005,62(1):1-15.
[15] Yu M,Cavero V,Lu Q,et al.Follicular helper T cells in rheumatoid arthritis[J].Clin Rheumatol,2015,34(9):1489-1493.
[16] Chen M,Guo Z,Ju W,et al.The development and function of follicular helper T cells in immune responses[J].Cell Mol Immunol,2012,9(5):375-379.
[17] Vincze K,Kolonics-Farkas A,Bohacs A,et al.Peripheral CD4+ T-cell changes in connective tissue diseases[J].Cytokine Growth Factor Rev,2018,8(11):62-67.
[2] Glant TT,Mikecz K,Rauch TA.Epigenetics in the pathogenesis of rheumatoid arthritis[J].BMC Med,2014,5(12):32-35.
[3] de Pablo P,Dietrich T,Chapple IL,et al.The autoantibody repertoire in periodontitis:a role in the induction of autoimmunity to citrullinated proteins in rheumatoid arthritis[J].Ann Rheum Dis,2014,73(3):580-586.
[4] Angelotti F,Parma A,Cafaro G,et al.One year in review 2017:pathogenesis of rheumatoid arthritis[J].Clin Exp Rheumatol,2017,35(3):368-378.
[5] Hauser B,Harre U.The Role of Autoantibodies in Bone Metabolism and Bone Loss[J].Calcif Tissue Int,2018,102(5):522-532.
[6] McInnes IB,Schett G.Pathogenetic insights from the treatment of rheumatoid arthritis[J].Lancet,2017,389(10086):2328-2337.
[7] Futo G,Somogyi A,Szekanecz Z.Visualization of DAS28,SDAI,and CDAI:the magic carpets of rheumatoid arthritis[J].Clin Rheumatol,2014,33(5):623-629.
[8] Bashford-Rogers RJM,Smith KGC,Thomas DC.Antibody repertoire analysis in polygenic autoimmune diseases[J].Immunology,2018,2(5):51-56
[9] Scherer HU,Huizinga TWJ,Kronke G,et al.The B cell response to citrullinated antigens in the development of rheumatoid arthritis[J].Nat Rev Rheumatol,2018,14(3):157-169.
[10] Wu H,Deng Y,Feng Y,et al.Epigenetic regulation in B-cell maturation and its dysregulation in autoimmunity[J].Cell Mol Immunol,2018,4(6):81-88.
[11] Pala O,Diaz A,Blomberg BB,et al.B Lymphocytes in Rheumatoid Arthritis and the Effects of Anti-TNF-alpha Agents on B Lymphocytes:A Review of the Literature[J].Clin Ther,2018,8(9):1023-1029.
[12] Benoist C,Mathis D.Treg cells,life history,and diversity[J].Cold Spring Harb Perspect Biol,2012,4(9):43-48.
[13] Cooles FA,Isaacs JD,Anderson AE.Treg cells in rheumatoid arthritis:an update[J].Curr Rheumatol Rep,2013,15(9):352-357.
[14] Wing K,Suri-Payer E,Rudin A.CD4+CD25+-regulatory T cells from mouse to man[J].Scand J Immunol,2005,62(1):1-15.
[15] Yu M,Cavero V,Lu Q,et al.Follicular helper T cells in rheumatoid arthritis[J].Clin Rheumatol,2015,34(9):1489-1493.
[16] Chen M,Guo Z,Ju W,et al.The development and function of follicular helper T cells in immune responses[J].Cell Mol Immunol,2012,9(5):375-379.
[17] Vincze K,Kolonics-Farkas A,Bohacs A,et al.Peripheral CD4+ T-cell changes in connective tissue diseases[J].Cytokine Growth Factor Rev,2018,8(11):62-67.