Potential for TCDD to induce regulatory functions in B cells as part of the mechanism for T cell suppression in EAE.
Potential for TCDD to induce regulatory functions in B cells as part of the mechanism for T cell suppression in EAE.
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DOI:
10.1016/j.taap.2022.116259
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发表时间:
2022-11-01
影响因子:
3.8
通讯作者:
Kaplan, Barbara L. F.
中科院分区:
文献类型:
--
作者:
McDonald, Amye;Nicaise, Ashleigh;Sears, Erin Rushing;Bell, Abigail;Kummari, Evangel;Kaplan, Barbara L. F.
Part of the mechanism by which 2,3,7.8-tetrachlorodibenzo-p-dioxin (TCDD) suppresses immune function involves induction of regulatory T cells and suppression of effector T cells. The goal of this project was to examine whether TCDD’s suppression of effector T cells was due in part to inducing B regulatory cells (Bregs). TCDD’s potential to increase the percentage and/or function of CD24+CD38+ B cells was assessed in response to lipopolysaccharide (LPS) + interleukin (IL)-4 in vitro and in a mild model of experimental autoimmune encephalomyelitis (EAE) in vivo. In vitro, TCDD did not consistently increase the percentage of CD19+CD24+CD38+ cells using splenocytes, purified B cells or bone marrow (BM) cells. However, TCDD increased IL-10 in all three culture preparations, and TCDD increased the percentage of CD5+CD24+CD38+ cells producing IL-10. In EAE, TCDD did not affect the percentage of the CD24+CD38+ cell population in CD19, B220 or CD5 B cells in splenocytes (SPLC), lymph nodes (LN) nor BM cells at end-stage disease. On the other hand, TCDD increased the CD19+CD24+CD38+ percentage in the spinal cord (SC) in EAE. Moreover, TCDD-treated B cells isolated from spleens or TCDD-treated BM cells in EAE mice modestly reduced the ability of naïve effector T cells to express interferon (IFN)-γ and tumor necrosis factor (TNF)-α. Together these data show that TCDD can induce regulatory functions in B cells, although it was not obvious simply by examining the expression of regulatory markers but by assessing function by cytokine production or mixed lymphocyte responses.
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DOI:
10.3390/antib11010004
发表时间:
2022-01-09
期刊:
Antibodies (Basel, Switzerland)
影响因子:
--
作者:
Nicaise AJ;McDonald A;Sears ER;Sturgis T;Kaplan BLF
通讯作者:
Kaplan BLF
影响因子:
4.5
作者:
Kummari E;Rushing E;Nicaise A;McDonald A;Kaplan BLF
通讯作者:
Kaplan BLF
影响因子:
4.4
作者:
Miyashita Y;Kouwaki T;Tsukamoto H;Okamoto M;Nakamura K;Oshiumi H
通讯作者:
Oshiumi H
影响因子:
3.7
作者:
Bunaciu RP;Jensen HA;MacDonald RJ;LaTocha DH;Varner JD;Yen A
通讯作者:
Yen A
影响因子:
3.7
作者:
Duarte JH;Di Meglio P;Hirota K;Ahlfors H;Stockinger B
通讯作者:
Stockinger B