Journal article
Regulatory IgDhi B Cells Suppress T Cell Function via IL-10 and PD-L1 during Progressive Visceral Leishmaniasis
The Journal of immunology (1950), Vol.196(10), pp.4100-4109
05/15/2016
DOI: 10.4049/jimmunol.1502678
PMCID: PMC4868652
PMID: 27076677
Abstract
During visceral leishmaniasis (VL), Th1-based inflammation is induced to control intracellular parasites. Inflammation-based pathology was shown to be dampened by IL-10 and eventual programmed death 1-mediated T cell exhaustion. Cell type(s) responsible for the initiation of T cell-produced IL-10 during VL are unknown. CD19(+), CD5(-), CD1d(-), IgD(hi) regulatory B cells from healthy controls produced IL-10 in the absence of infection or stimulation, in contrast to IgD(lo/neg) B cells. IgD(hi) B cells may have a de novo versus induced regulatory program. The population of IgD(hi) B cells increased 3-fold as VL progressed. B cells from VL dogs were necessary and sufficient to suppress Th1 cell effector function. IgD(hi) B cells induced IL-10 production by T cells and IgD(lo) B cells. Blockage of B cell-specific PD-L1 restored Th1 responses. IgD(hi) regulatory B cells represent a novel regulatory B cell that may precipitate T cell exhaustion during VL.
Details
- Title: Subtitle
- Regulatory IgDhi B Cells Suppress T Cell Function via IL-10 and PD-L1 during Progressive Visceral Leishmaniasis
- Creators
- Robert G Schaut - Department of Epidemiology, University of Iowa College of Public Health, Iowa City, IA 52242Ian M Lamb - Department of Epidemiology, University of Iowa College of Public Health, Iowa City, IA 52242Angela J Toepp - Department of Epidemiology, University of Iowa College of Public Health, Iowa City, IA 52242Benjamin Scott - Department of Epidemiology, University of Iowa College of Public Health, Iowa City, IA 52242Carolina O Mendes-Aguiar - Department of Biochemistry, Health Graduate Program, Institute of Tropical Medicine, Federal University of Rio Grande do Norte, Natal 1655, 59072-970, Brazil; Laboratório Interdisciplinar de Pesquisas Médicas, Instituto Oswaldo Cruz, Fiocruz, Rio de Janeiro 4365, 21045-900, BrazilJose F V Coutinho - Department of Biochemistry, Health Graduate Program, Institute of Tropical Medicine, Federal University of Rio Grande do Norte, Natal 1655, 59072-970, Brazil; Center for Zoonosis, Health Secretariat, Natal 1655, 59072-970, Brazil; andSelma M B Jeronimo - Department of Biochemistry, Health Graduate Program, Institute of Tropical Medicine, Federal University of Rio Grande do Norte, Natal 1655, 59072-970, BrazilMary E Wilson - Immunology Program, University of Iowa Carver College of Medicine, Iowa City, IA 52242John T Harty - Immunology Program, University of Iowa Carver College of Medicine, Iowa City, IA 52242Thomas J Waldschmidt - Immunology Program, University of Iowa Carver College of Medicine, Iowa City, IA 52242Christine A Petersen - Department of Epidemiology, University of Iowa College of Public Health, Iowa City, IA 52242; Immunology Program, University of Iowa Carver College of Medicine, Iowa City, IA 52242 christine-petersen@uiowa.edu
- Resource Type
- Journal article
- Publication Details
- The Journal of immunology (1950), Vol.196(10), pp.4100-4109
- DOI
- 10.4049/jimmunol.1502678
- PMID
- 27076677
- PMCID
- PMC4868652
- NLM abbreviation
- J Immunol
- ISSN
- 0022-1767
- eISSN
- 1550-6606
- Publisher
- United States
- Grant note
- S10 RR027219 / NCRR NIH HHS I01 BX001983 / BLRD VA P30 CA086862 / NCI NIH HHS P50 AI030639 / NIAID NIH HHS
- Language
- English
- Date published
- 05/15/2016
- Academic Unit
- Microbiology and Immunology; Infectious Diseases; International Programs; Epidemiology; Pathology; Internal Medicine
- Record Identifier
- 9983996096902771
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