| [1] |
Cancro MP. Age⁃associated B cells[J]. Annu Rev Immunol, 2020,38:315⁃340. DOI: 10.1146/annurev⁃immunol⁃092419⁃031130.
|
| [2] |
Mouat IC, Goldberg E, Horwitz MS. Age⁃associated B cells in autoimmune diseases[J]. Cell Mol Life Sci, 2022,79(8):402. DOI: 10.1007/s00018⁃022⁃04433⁃9.
|
| [3] |
Hao Y, O'Neill P, Naradikian MS, et al. A B⁃cell subset uniquely responsive to innate stimuli accumulates in aged mice[J]. Blood, 2011,118(5):1294⁃1304. DOI: 10.1182/blood⁃2011⁃01⁃330530.
|
| [4] |
Rubtsov AV, Rubtsova K, Fischer A, et al. Toll⁃like receptor 7 (TLR7)⁃driven accumulation of a novel CD11c⁺ B⁃cell population is important for the development of autoimmunity[J]. Blood, 2011,118(5):1305⁃1315. DOI: 10.1182/blood⁃2011⁃01⁃331462.
|
| [5] |
Saadoun D, Terrier B, Bannock J, et al. Expansion of autoreactive unresponsive CD21⁃/low B cells in Sjögren's syndrome⁃associated lymphoproliferation[J]. Arthritis Rheum, 2013,65(4):1085⁃1096. DOI: 10.1002/art.37828.
|
| [6] |
Liu Y, Zhou S, Qian J, et al. T⁃bet+CD11c+ B cells are critical for antichromatin immunoglobulin G production in the development of lupus[J]. Arthritis Res Ther, 2017,19(1):225. DOI: 10.1186/s13075⁃017⁃1438⁃2.
|
| [7] |
Holla P, Dizon B, Ambegaonkar AA, et al. Shared transcriptional profiles of atypical B cells suggest common drivers of expansion and function in malaria, HIV, and autoimmunity[J]. Sci Adv, 2021,7(22):eabg8384. DOI: 10.1126/sciadv.abg8384.
|
| [8] |
Ratliff M, Alter S, Frasca D, et al. In senescence, age⁃associated B cells secrete TNFα and inhibit survival of B⁃cell precursors[J]. Aging Cell, 2013,12(2):303⁃311. DOI: 10.1111/acel.12055.
|
| [9] |
Ricker E, Manni M, Flores⁃Castro D, et al. Altered function and differentiation of age⁃associated B cells contribute to the female bias in lupus mice[J]. Nat Commun, 2021,12(1):4813. DOI: 10.1038/s41467⁃021⁃25102⁃8.
|
| [10] |
Mouat IC, Horwitz MS. Age⁃associated B cells in viral infection[J]. PLoS Pathog, 2022,18(3):e1010297. DOI: 10.1371/journal.ppat.1010297.
|
| [11] |
Mouat IC, Morse ZJ, Shanina I, et al. Latent gammaherpesvirus exacerbates arthritis through modification of age⁃associated B cells[J]. Elife, 2021,10:e67024. DOI: 10.7554/eLife.67024.
|
| [12] |
Jenks SA, Cashman KS, Zumaquero E, et al. Distinct effector B cells induced by unregulated Toll⁃like receptor 7 contribute to pathogenic responses in systemic lupus erythematosus[J]. Immunity, 2018,49(4):725⁃739.e6. DOI: 10.1016/j.immuni. 2018.08.015.
|
| [13] |
Brown GJ, Cañete PF, Wang H, et al. TLR7 gain⁃of⁃function genetic variation causes human lupus[J]. Nature, 2022,605(7909):349⁃356. DOI: 10.1038/s41586⁃022⁃04642⁃z.
|
| [14] |
Rubtsov AV, Rubtsova K, Kappler JW, et al. TLR7 drives accumulation of ABCs and autoantibody production in autoimmune⁃prone mice[J]. Immunol Res, 2013,55(1⁃3):210⁃216. DOI: 10.1007/s12026⁃012⁃8365⁃8.
|
| [15] |
Leibler C, John S, Elsner RA, et al. Genetic dissection of TLR9 reveals complex regulatory and cryptic proinflammatory roles in mouse lupus[J]. Nat Immunol, 2022,23(10):1457⁃1469. DOI: 10.1038/s41590⁃022⁃01310⁃2.
|
| [16] |
Naradikian MS, Myles A, Beiting DP, et al. Cutting edge: IL⁃4, IL⁃21, and IFN⁃γ interact to govern T⁃bet and CD11c expression in TLR⁃activated B cells[J]. J Immunol, 2016,197(4):1023⁃1028. DOI: 10.4049/jimmunol.1600522.
|
| [17] |
Gao M, Liu S, Chatham WW, et al. IL⁃4⁃induced quiescence of resting naive B cells is disrupted in systemic lupus erythematosus[J]. J Immunol, 2022,209(8):1513⁃1522. DOI: 10.4049/jimmunol. 2200409.
|
| [18] |
Zhu Y, Tang X, Xu Y, et al. RNASE2 mediates age⁃associated B cell expansion through monocyte derived IL⁃10 in patients with systemic lupus erythematosus[J]. Front Immunol, 2022,13:752189. DOI: 10.3389/fimmu.2022.752189.
|
| [19] |
Song W, Antao OQ, Condiff E, et al. Development of Tbet⁃ and CD11c⁃expressing B cells in a viral infection requires T follicular helper cells outside of germinal centers[J]. Immunity, 2022,55(2):290⁃307.e5. DOI: 10.1016/j.immuni.2022.01.002.
|
| [20] |
Levack RC, Newell KL, Popescu M, et al. CD11c(+) T⁃bet(+) B cells require IL⁃21 and IFN⁃γ from type 1 T follicular helper cells and intrinsic Bcl⁃6 expression but develop normally in the absence of T⁃bet[J]. J Immunol, 2020,205(4):1050⁃1058. DOI: 10.4049/jimmunol.2000206.
|
| [21] |
Keller B, Strohmeier V, Harder I, et al. The expansion of human T⁃bet(high)CD21(low) B cells is T cell dependent[J]. Sci Immunol, 2021,6(64):eabh0891. DOI: 10.1126/sciimmunol.abh0891.
|
| [22] |
Wang S, Wang J, Kumar V, et al. IL⁃21 drives expansion and plasma cell differentiation of autoreactive CD11c(hi)T⁃bet(+) B cells in SLE[J]. Nat Commun, 2018,9(1):1758. DOI: 10.1038/s41467⁃018⁃03750⁃7.
|
| [23] |
Murakami Y, Fukui R, Tanaka R, et al. Anti⁃TLR7 antibody protects against lupus nephritis in NZBWF1 mice by targeting B cells and patrolling monocytes[J]. Front Immunol, 2021,12:777197. DOI: 10.3389/fimmu.2021.777197.
|
| [24] |
Claes N, Fraussen J, Vanheusden M, et al. Age⁃associated B cells with proinflammatory characteristics are expanded in a proportion of multiple sclerosis patients[J]. J Immunol, 2016,197(12):4576⁃4583. DOI: 10.4049/jimmunol.1502448.
|
| [25] |
Rubtsov AV, Rubtsova K, Kappler JW, et al. CD11c⁃expressing B cells are located at the T cell/B cell border in spleen and are potent APCs[J]. J Immunol, 2015,195(1):71⁃79. DOI: 10. 4049/jimmunol.1500055.
|
| [26] |
Wang Z, Wang Z, Wang J, et al. T⁃bet⁃expressing B cells are positively associated with Crohn's disease activity and support Th1 inflammation[J]. DNA Cell Biol, 2016,35(10):628⁃635. DOI: 10.1089/dna.2016.3304.
|
| [27] |
Zhang W, Zhang H, Liu S, et al. Excessive CD11c+Tbet+ B cells promote aberrant TFH differentiation and affinity⁃based germinal center selection in lupus[J]. Proc Natl Acad Sci U S A, 2019,116(37):18550⁃18560. DOI: 10.1073/pnas.1901340116.
|
| [28] |
Manni M, Gupta S, Ricker E, et al. Regulation of age⁃associated B cells by IRF5 in systemic autoimmunity[J]. Nat Immunol, 2018,19(4):407⁃419. DOI: 10.1038/s41590⁃018⁃0056⁃8.
|
| [29] |
Wu C, Fu Q, Guo Q, et al. Lupus⁃associated atypical memory B cells are mTORC1⁃hyperactivated and functionally dysregulated[J]. Ann Rheum Dis, 2019,78(8):1090⁃1100. DOI: 10.1136/annrheumdis⁃2019⁃215039.
|
| [30] |
Wehr C, Eibel H, Masilamani M, et al. A new CD21low B cell population in the peripheral blood of patients with SLE[J]. Clin Immunol, 2004,113(2):161⁃171. DOI: 10.1016/j.clim.2004. 05.010.
|
| [31] |
Rincon⁃Arevalo H, Wiedemann A, Stefanski AL, et al. Deep phenotyping of CD11c+ B cells in systemic autoimmunity and controls[J]. Front Immunol, 2021,12:635615. DOI: 10.3389/fimmu.2021.635615.
|
| [32] |
Hurtado C, Rojas⁃Gualdrón DF, Urrego R, et al. Altered B cell phenotype and CD27+ memory B cells are associated with clinical features and environmental exposure in Colombian systemic lupus erythematosus patients[J]. Front Med (Lausanne), 2022,9:950452. DOI: 10.3389/fmed.2022.950452.
|
| [33] |
Faustini F, Sippl N, Stålesen R, et al. Rituximab in systemic lupus erythematosus: transient effects on autoimmunity associated lymphocyte phenotypes and implications for immunogenicity[J]. Front Immunol, 2022,13:826152. DOI: 10.3389/fimmu.2022.826152.
|
| [34] |
Ramsköld D, Parodis I, Lakshmikanth T, et al. B cell alterations during BAFF inhibition with belimumab in SLE[J]. EBioMedicine, 2019,40:517⁃527. DOI: 10.1016/j.ebiom.2018.12.035.
|
| [35] |
Li ZY, Cai ML, Qin Y, et al. Age/autoimmunity⁃associated B cells in inflammatory arthritis: an emerging therapeutic target[J]. Front Immunol, 2023,14:1103307. DOI: 10.3389/fimmu.2023. 1103307.
|
| [36] |
Bao W, Xie M, Ye Y. Age⁃associated B cells indicate disease activity in rheumatoid arthritis[J]. Cell Immunol, 2022,377:104533. DOI: 10.1016/j.cellimm.2022.104533.
|
| [37] |
Thorarinsdottir K, Camponeschi A, Jonsson C, et al. CD21⁃/low B cells associate with joint damage in rheumatoid arthritis patients[J]. Scand J Immunol, 2019,90(2):e12792. DOI: 10. 1111/sji.12792.
|
| [38] |
Vidal⁃Pedrola G, Naamane N, Cameron JA, et al. Characterization of age⁃associated B cells in early drug⁃naïve rheumatoid arthritis patients[J]. Immunology, 2023,168(4):640⁃653. DOI: 10.1111/imm.13598.
|
| [39] |
Wing E, Sutherland C, Miles K, et al. Double⁃negative⁃2 B cells are the major synovial plasma cell precursor in rheumatoid arthritis[J]. Front Immunol, 2023,14:1241474. DOI: 10.3389/fimmu.2023.1241474.
|
| [40] |
Qin Y, Cai ML, Jin HZ, et al. Age⁃associated B cells contribute to the pathogenesis of rheumatoid arthritis by inducing activation of fibroblast⁃like synoviocytes via TNF⁃α⁃mediated ERK1/2 and JAK⁃STAT1 pathways[J]. Ann Rheum Dis, 2022,81(11):1504⁃1514. DOI: 10.1136/ard⁃2022⁃222605.
|
| [41] |
Wilbrink R, Spoorenberg A, Arends S, et al. CD27⁃CD38lowCD21low B⁃cells are increased in axial spondyloarthritis[J]. Front Immunol, 2021,12:686273. DOI: 10.3389/fimmu.2021.686273.
|
| [42] |
Wilfong EM, Vowell KN, Bunn KE, et al. CD19 + CD21lo/neg cells are increased in systemic sclerosis⁃associated interstitial lung disease[J]. Clin Exp Med, 2022,22(2):209⁃220. DOI: 10.1007/s10238⁃021⁃00745⁃5.
|
| [43] |
Dai D, Gu S, Han X, et al. The transcription factor ZEB2 drives the formation of age⁃associated B cells[J]. Science, 2024,383(6681):413⁃421. DOI: 10.1126/science.adf8531.
|
| [44] |
Levack RC, Newell KL, Cabrera⁃Martinez B, et al. Adenosine receptor 2a agonists target mouse CD11c+T⁃bet+ B cells in infection and autoimmunity[J]. Nat Commun, 2022,13(1):452. DOI: 10.1038/s41467⁃022⁃28086⁃1.
|