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CD1d-dependent immune suppression mediated by regulatory B cells through modulations of iNKT cells
- Source :
- Nature Communications, Vol 9, Iss 1, Pp 1-17 (2018)
- Publication Year :
- 2018
- Publisher :
- Nature Publishing Group, 2018.
-
Abstract
- Regulatory B cells (Breg) express high levels of CD1d that presents lipid antigens to invariant natural killer T (iNKT) cells. The function of CD1d in Breg biology and iNKT cell activity during inflammation remains unclear. Here we show, using chimeric mice, cell depletion and adoptive cell transfer, that CD1d–lipid presentation by Bregs induces iNKT cells to secrete interferon (IFN)-γ to contribute, partially, to the downregulation of T helper (Th)1 and Th17-adaptive immune responses and ameliorate experimental arthritis. Mice lacking CD1d-expressing B cells develop exacerbated disease compared to wild-type mice, and fail to respond to treatment with the prototypical iNKT cell agonist α-galactosylceramide. The absence of lipid presentation by B cells alters iNKT cell activation with disruption of metabolism regulation and cytokine responses. Thus, we identify a mechanism by which Bregs restrain excessive inflammation via lipid presentation.
- Subjects :
- 0301 basic medicine
Male
Adoptive cell transfer
Regulatory B cells
medicine.medical_treatment
Science
General Physics and Astronomy
Galactosylceramides
chemical and pharmacologic phenomena
General Biochemistry, Genetics and Molecular Biology
03 medical and health sciences
Interferon-gamma
Immune system
Interferon
medicine
Animals
lcsh:Science
Cells, Cultured
Mice, Knockout
B-Lymphocytes
B-Lymphocytes, Regulatory
Multidisciplinary
biology
Chemistry
General Chemistry
Th1 Cells
Natural killer T cell
Adoptive Transfer
Arthritis, Experimental
3. Good health
Cell biology
Mice, Inbred C57BL
030104 developmental biology
Cytokine
CD1D
biology.protein
Natural Killer T-Cells
Th17 Cells
lipids (amino acids, peptides, and proteins)
lcsh:Q
Antigens, CD1d
Cell activation
medicine.drug
Subjects
Details
- Language :
- English
- ISSN :
- 20411723
- Volume :
- 9
- Issue :
- 1
- Database :
- OpenAIRE
- Journal :
- Nature Communications
- Accession number :
- edsair.doi.dedup.....951be7b22d632fc910c70ac4bef7c954