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Nat Immunol. 2018 Sep;19(9):1025-1034. doi: 10.1038/s41590-018-0177-0. Epub 2018 Aug 6.

IL-9 receptor signaling in memory B cells regulates humoral recall responses.

Author information

1
Division of Molecular Biology, Research Institute for Biomedical Sciences (RIBS), Tokyo University of Science, Noda, Japan.
2
Department of Chemotherapy and Mycoses, National Institute of Infectious Diseases, Tokyo, Japan.
3
Ludwig Institute for Cancer Research and Experimental Medicine Unit, Universite catholique de Louvain, Brussels, Belgium.
4
Division of Molecular Biology, Research Institute for Biomedical Sciences (RIBS), Tokyo University of Science, Noda, Japan. kitamura@rs.noda.tus.ac.jp.

Abstract

Memory B cells (Bmem cells) are the basis of long-lasting humoral immunity. They respond to re-encountered antigens by rapidly producing specific antibodies and forming germinal centers (GCs), a recall response that has been known for decades but remains poorly understood. We found that the receptor for the cytokine IL-9 (IL-9R) was induced selectively on Bmem cells after primary immunization and that IL-9R-deficient mice exhibited a normal primary antibody response but impaired recall antibody responses, with attenuated population expansion and plasma-cell differentiation of Bmem cells. In contrast, there was augmented GC formation, possibly due to defective downregulation of the ligand for the co-stimulatory receptor ICOS on Bmem cells. A fraction of Bmem cells produced IL-9. These findings indicate that IL-9R signaling in Bmem cells regulates humoral recall responses.

PMID:
30082831
DOI:
10.1038/s41590-018-0177-0
[Indexed for MEDLINE]

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