Journal
NATURE IMMUNOLOGY
Volume 19, Issue 12, Pages 1341-+Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41590-018-0237-5
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Funding
- Deutsche Forschungsgemeinschaft [SFB1054-B06, TRR128]
- German Ministry of Education and Research (BMBF, T-B in NMO)
- ERC [CoG 647215]
- Technical University of Munich
- Deutsche Forschungsgemeinschaft (Synergy)
- Swiss National Science Foundation
- Deutsche Forschungsgemeinschaft (Kompetenznetz Multiple Sklerose KKNMS)
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Polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs) have been characterized in the context of malignancies. Here we show that PMN-MDSCs can restrain B cell accumulation during central nervous system (CNS) autoimmunity. Ly6G(+) cells were recruited to the CNS during experimental autoimmune encephalomyelitis (EAE), interacted with B cells that produced the cytokines GM-CSF and interleukin-6 (IL-6), and acquired properties of PMN-MDSCs in the CNS in a manner dependent on the signal transducer STAT3. Depletion of Ly6G(+) cells or dysfunction of Ly6G(+) cells through conditional ablation of STAT3 led to the selective accumulation of GM-CSF-producing B cells in the CNS compartment, which in turn promoted an activated microglial phenotype and lack of recovery from EAE. The frequency of CD138(+) B cells in the cerebrospinal fluid (CSF) of human subjects with multiple sclerosis was negatively correlated with the frequency of PMN-MDSCs in the CSF. Thus PMN-MDSCs might selectively control the accumulation and cytokine secretion of B cells in the inflamed CNS.
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