期刊
LUPUS
卷 28, 期 11, 页码 1337-1343出版社
SAGE PUBLICATIONS LTD
DOI: 10.1177/0961203319869468
关键词
Belimumab; transitional B cells; translational; systemic lupus erythematosus; human B-cell production
类别
资金
- Transplantation Institute Loma Linda University Health Care
- Loma Linda University School of Medicine
- NIH [P20 MD006988, 2R25 GM060507]
- Bevra-Hahn Scholarship Award
- Loma Linda University School of Medicine-Rheumatology Division Research Endowment Fund
Objective:We evaluated the effects of the B-cell activating factor (BAFF)-targeting antibody Belimumab on human nonmemory B-cell pools. Human B-cell pools were identified using surface markers adapted from mouse studies that specifically assessed reductions in immature B cells due to BAFF depletion. Patients with systemic lupus erythematosus (SLE) have high levels of both BAFF and immature B cells. Mechanistic mouse studies provide a framework for understanding human responses to therapies that target B cells. Methods:Peripheral blood mononuclear cells were isolated from healthy donors and SLE patients on Belimumab or standard-of-care therapy (SCT). Cells were stained for flow cytometry to identify B-cell subsets based on CD21/CD24. Differences in subset proportions were determined by one-way ANOVA and Tukey's post hoc test. Results:Patients treated with Belimumab show alterations in the nonmemory B-cell pool characterized by a decrease in the Transitional 2 (T2) subset (p = 0.002), and an increase in the proportion of Transitional 1 (T1) cells (p = 0.005) as compared with healthy donors and SCT patients. The naive B-cell compartment showed no significant differences between the groups (p = 0.293). Conclusion:Using a translational approach, we show that Belimumab-mediated BAFF depletion reduces the T2 subset in patients, similar to observations in mouse models with BAFF depletion.
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