B细胞在骨破坏性疾病中作用的研究进展

doi:10.13591/j.cnki.kqyx.2022.10.011

摘要/Abstract

摘要： 骨骼系统与免疫系统密切相关,B细胞作为免疫系统的重要组成部分,通过RANKL/RANK/OPG轴、分泌细胞因子和抗体等方式直接或间接地调控骨稳态,在骨破坏性疾病的发生发展中发挥关键作用。本文就B细胞和骨组织的关系及B细胞在骨破坏性疾病中的作用作一综述,为骨破坏性疾病的研究和治疗提供新思路。

关键词: B细胞, 骨破坏性疾病, 类风湿性关节炎, 牙周炎, 骨质疏松症

Abstract: There is a close relationship between the skeletal system and the immune system. As an important part of the immune system, B lymphocytes regulate bone homeostasis through the RANKL/RANK/OPG axis and the production of cytokines and antibodies, which play a key role in the occurrence and development of bone destructive diseases. This review will discuss the interaction between B lymphocytes and bone homeostasis and the role of B lymphocytes in bone destructive diseases, hoping to provide new ideas for research and treatment of bone destructive diseases.

Key words: B lymphocyte, bone destructive disease, rheumatoid arthritis, periodontitis, osteoporosis

中图分类号:

张滨婧, 张璟岚, 张辰玥, 陈艺菲, 胡芝爱. B细胞在骨破坏性疾病中作用的研究进展[J]. 口腔医学, 2022, 42(10): 922-927.

ZHANG Binjing, ZHANG Jinglan, ZHANG Chenyue, CHEN Yifei, HU Zhi′ai. Progress of research on the role of B lymphocytes in bone destructive diseases[J]. Stomatology, 2022, 42(10): 922-927.

参考文献

[1] Kim JM, Lin CJ, Stavre Z, et al. Osteoblast-osteoclast communication and bone homeostasis[J]. Cells, 2020, 9(9):2073.
[2] Arron JR, Choi Y. Bone versus immune system[J]. Nature, 2000, 408(6812):535-536.
[3] Takeuchi Y, Hirota K, Sakaguchi S. Impaired T cell receptorsignaling and development of T cell-mediated autoimmune arthritis[J]. Immunol Rev, 2020, 294(1):164-176.
[4] Figueredo CM, Lira-Junior R, Love RM. T and B cells in periodontal disease:New functions in a complex scenario[J]. Int J Mol Sci, 2019, 20(16):3949.
[5] Zehentmeier S, Pereira JP. Cell circuits and niches controlling B cell development[J]. Immunol Rev, 2019, 289(1):142-157.
[6] Nagasawa T. Microenvironmental niches in the bone marrow required for B-cell development[J]. Nat Rev Immunol, 2006, 6(2):107-116.
[7] Minami H, Nagaharu K, Nakamori Y, et al. CXCL12-CXCR4 axis is required for contact-mediated human B lymphoid and plasmacytoid dendritic cell differentiation but not T lymphoid generation[J]. J Immunol, 2017, 199(7):2343-2355.
[8] Honczarenko M, Douglas RS, Mathias C, et al. SDF-1 responsiveness does not correlate with CXCR4 expression levels of developing human bone marrow B cells[J]. Blood, 1999, 94(9):2990-2998.
[9] Honczarenko M, Glodek AM, Swierkowski M, et al. Developmen-tal stage-specific shift in responsiveness to chemokines during human B-cell development[J]. Exp Hematol, 2006, 34(8):1093-1100.
[10] Mcheik S, van Eeckhout N, de Poorter C, et al. Coexpression of CCR7 and CXCR4 during B cell development controls CXCR4 responsiveness and bone marrow homing[J]. Front Immunol, 2019, 10:2970.
[11] Valenzona HO, Pointer R, Ceredig R, et al. Prelymphomatous B cell hyperplasia in the bone marrow of interleukin-7 transgenic mice:Precursor B cell dynamics, microenvironmental organization and osteolysis[J]. Exp Hematol, 1996, 24(13):1521-1529.
[12] Opferman JT, Letai A, Beard C, et al. Development and maintenance of B and T lymphocytes requires antiapoptotic MCL-1[J]. Nature, 2003, 426(6967):671-676.
[13] Yu M, Chen YH, Zeng H, et al. PLCγ-dependent mTOR signalling controls IL-7-mediated early B cell development[J]. Nat Commun, 2017, 8(1):1457.
[14] Clark MR, Mandal M, Ochiai K, et al. Orchestrating B cell lymphopoiesis through interplay of IL-7 receptor and pre-B cell receptor signalling[J]. Nat Rev Immunol, 2014, 14(2):69-80.
[15] Ochiai K, Maienschein-Cline M, Mandal M, et al. A self-reinforcing regulatory network triggered by limiting IL-7 activates pre-BCR signaling and differentiation[J]. Nat Immunol, 2012, 13(3):300-307.
[16] Fistonich C, Zehentmeier S, Bednarski JJ, et al. Cell circuits between B cell progenitors and IL-7⁺ mesenchymal progenitor cells control B cell development[J]. J Exp Med, 2018, 215(10):2586-2599.
[17] Dougall WC, Glaccum M, Charrier K, et al. RANK is essential for osteoclast and lymph node development[J]. GenesDev, 1999, 13(18):2412-2424.
[18] Stolina M, Dwyer D, Ominsky MS, et al. Continuous RANKL inhibition in osteoprotegerin transgenic mice and rats suppresses bone resorption without impairing lymphorganogenesis or functional immune responses[J]. J Immunol, 2007, 179(11):7497-7505.
[19] Driessen RL, Johnston HM, Nilsson SK. Membrane-bound stem cell factor is a key regulator in the initial lodgment of stem cells within the endosteal marrow region[J]. ExpHematol, 2003, 31(12):1284-1291.
[20] Giampaolo S, Wójcik G, Klein-Hessling S, et al. B cell development is critically dependent on NFATc₁ activity[J]. Cell Mol Immunol, 2019, 16(5):508-520.
[21] Gwin KA, Shapiro MB, Dolence JJ, et al. Hoxa9 and Flt3 signaling synergistically regulate an early checkpoint in lymphopoiesis[J]. J Immunol, 2013, 191(2):745-754.
[22] Yee CS, Manilay JO, Chang JC, et al. Conditional deletion of sost in MSC-derived lineages identifies specific cell-type contributions to bone mass and B-cell development[J]. J Bone Miner Res, 2018, 33(10):1748-1759.
[23] Zhu J, Garrett R, Jung Y, et al. Osteoblasts support B-lymphocyte commitment and differentiation from hematopoietic stem cells[J]. Blood, 2007, 109(9):3706-3712.
[24] Martin SK, Fitter S, El Khawanky N, et al. mTORC1 plays an important role in osteoblastic regulation of B-lymphopoiesis[J]. Sci Rep, 2018, 8(1):14501.
[25] Wang YK, Xiao M, Tao C, et al. Inactivation of mTORC1 signaling in osterix-expressing cells impairs B-cell differentiation[J]. J Bone Miner Res, 2018, 33(4):732-742.
[26] Mansour A, Anginot A, Mancini SJC, et al. Osteoclast activity modulates B-cell development in the bone marrow[J]. Cell Res, 2011, 21(7):1102-1115.
[27] Geffroy-Luseau A, Jégo G, Bataille R, et al. Osteoclasts support the survival of human plasma cells in vitro[J]. Int Immunol, 2008, 20(6):775-782.
[28] Li Y, Toraldo G, Li AM, et al. B cells and T cells are critical for the preservation of bone homeostasis and attainment of peak bone mass in vivo[J]. Blood, 2007, 109(9):3839-3848.
[29] Cawley KM, Bustamante-Gomez NC, Guha AG, et al. Local production of osteoprotegerin by osteoblasts suppresses bone resorption[J]. Cell Rep, 2020, 32(10):108052.
[30] Kolomansky A, Kaye I, Ben-Califa N, et al. Anti-CD20-mediated B cell depletion is associated with bone preservation in lymphoma patients and bone mass increase in mice[J]. Front Immunol, 2020, 11:561294.
[31] Cao JJ, Wang SM, Wei CM, et al. Agrimophol suppresses RANKL-mediated osteoclastogenesis through Blimp1-Bcl6 axis and prevents inflammatory bone loss in mice[J]. Int Immunopharma-col, 2021, 90:107137.
[32] Jarry CR, Duarte PM, Freitas FF, et al. Secreted osteoclastogenic factor of activated T cells (SOFAT), a novel osteoclast activator, in chronic periodontitis[J]. Hum Immunol, 2013, 74(7):861-866.
[33] Audzevich T, Bashford-Rogers R, Mabbott NA, et al. Pre/pro-B cells generate macrophage populations during homeostasis and inflammation[J]. Proc Natl Acad Sci USA, 2017, 114(20):E3954-E3963.
[34] Deshet-Unger N, Kolomansky A, Ben-Califa N, et al. Erythropoietin receptor in B cells plays a role in bone remodeling in mice[J]. Theranostics, 2020, 10(19):8744-8756.
[35] Okamoto K, Takayanagi H. Osteoimmunology[J]. Cold Spring Harb Perspect Med, 2019, 9(1):a031245.
[36] Engdahl C, Bang H, Dietel K, et al. Periarticular bone loss in arthritis is induced by autoantibodies against citrullinated vimentin[J]. J Bone Miner Res, 2018, 33(12):2243.
[37] Germar K, Fehres CM, Scherer HU, et al. Generation and characterization of anti-citrullinated protein antibody-producing B cell clones from rheumatoid arthritis patients[J]. Arthritis Rheumatol, 2019, 71(3):340-350.
[38] Mahendra A, Yang XY, Abnouf S, et al. Beyond autoantibodies:Biologic roles of human autoreactive B cells in rheumatoid arthritis revealed by RNA-sequencing[J]. Arthritis Rheumatol, 2019, 71(4):529-541.
[39] Yeo L, Toellner KM, Salmon M, et al. Cytokine mRNA profiling identifies B cells as a major source of RANKL in rheumatoid arthritis[J]. Ann Rheum Dis, 2011, 70(11):2022-2028.
[40] Meednu N, Zhang HW, Owen T, et al. Production of RANKL by memory B cells:A link between B cells and bone erosion in rheumatoid arthritis[J]. Arthritis Rheumatol, 2016, 68(4):805-816.
[41] Sun W, Meednu N, Rosenberg A, et al. B cells inhibit bone formation in rheumatoid arthritis by suppressing osteoblast differentiation[J]. Nat Commun, 2018, 9(1):5127.
[42] Noack M, Miossec P. Selected cytokine pathways in rheumatoid arthritis[J]. Semin Immunopathol, 2017, 39(4):365-383.
[43] Mahanonda R, Champaiboon C, Subbalekha K, et al. Human memory B cells in healthy gingiva, gingivitis, and periodontitis[J]. J Immunol, 2016, 197(3):715-725.
[44] Han YK, Jin Y, Miao YB, et al. Improved RANKL production by memory B cells:A way for B cells promote alveolar bone destruction during periodontitis[J]. Int Immunopharmacol, 2018, 64:232-237.
[45] Jarry CR, Martinez EF, Peruzzo DC, et al. Expression of SOFAT by T- and B-lineage cells may contribute to bone loss[J]. Mol Med Rep, 2016, 13(5):4252-4258.
[46] Ahmed A, Koma MK. Interleukin-33 triggers B1 cell expansion and its release of monocyte/macrophage chemoattractants and growth factors[J]. Scand J Immunol, 2015, 82(2):118-124.
[47] Zhang XQ, Jin Y, Wang QX, et al. Autophagy-mediated regulation patterns contribute to the alterations of the immune microenvironment in periodontitis[J]. Aging, 2020, 13(1):555-577.
[48] 曹国琴, 林江. B10细胞与牙周炎免疫调控的研究进展[J]. 口腔医学, 2019, 39(8):748-752.
[49] Wang YH, Yu XQ, Lin J, et al. B10 cells alleviate periodontal bone loss in experimental periodontitis[J]. Infect Immun, 2017, 85(9):e00335-17.
[50] Hu Y, Yu P, Yu XB, et al. IL-21/anti-Tim1/CD40 ligand promotes B10 activity in vitro and alleviates bone loss in experimental periodontitis in vivo[J]. Biochim Biophys Acta Mol Basis Dis, 2017, 1863(9):2149-2157.
[51] Phiel KL, Henderson RA, Adelman SJ, et al. Differential estrogen receptor gene expression in human peripheral blood mononuclear cell populations[J]. Immunol Lett, 2005, 97(1):107-113.
[52] Xiao P, Chen Y, Jiang H, et al. In vivo genome-wide expression study on human circulating B cells suggests a novel ESR1 and MAPK₃ network for postmenopausal osteoporosis[J]. J Bone Miner Res, 2008, 23(5):644-654.
[53] Ponte F, Kim HN, Iyer S, et al. Cxcl12 deletion in mesenchymal cells increases bone turnover and attenuates the loss of cortical bone caused by estrogen deficiency in mice[J]. J Bone Miner Res, 2020, 35(8):1441-1451.
[54] Fujiwara Y, Piemontese M, Liu Y, et al. RANKL (receptor activator of NFκB ligand) produced by osteocytes is required for the increase in B cells and bone loss caused by estrogen deficiency in mice[J]. J Biol Chem, 2016, 291(48):24838-24850.
[55] Breuil V, Ticchioni M, Testa J, et al. Immune changes in post-menopausal osteoporosis:The Immunos study[J]. Osteoporos Int, 2010, 21(5):805-814.
[56] Brown TT, Qaqish RB. Antiretroviral therapy and the prevalence of osteopenia and osteoporosis:A meta-analytic review[J]. AIDS, 2006, 20(17):2165-2174.
[57] Titanji K, Vunnava A, Sheth AN, et al. Dysregulated B cell expression of RANKL and OPG correlates with loss of bone mineral density in HIV infection[J]. PLoS Pathog, 2014, 10(10):e1004497.
[58] Titanji K, Ofotokun I, Weitzmann MN. Immature/transitional B-cell expansion is associated with bone loss in HIV-infected individuals with severe CD4⁺ T-cell lymphopenia[J]. AIDS, 2020, 34(10):1475-1483.
[59] Li W, Wei C, Xu L, et al. Schistosome infection promotes osteoclast-mediated bone loss[J]. PLoS Pathog, 2021, 17(3):e1009462.