Journal
INTERNATIONAL IMMUNOLOGY
Volume 23, Issue 4, Pages 261-269Publisher
OXFORD UNIV PRESS
DOI: 10.1093/intimm/dxq478
Keywords
CCR6; CD11c(int) B cells; cell differentiation; M cells; Peyer's patch
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Funding
- Ministry of Education, Culture, Sports, Science and Technology of Japan [22689017, 18790343, 20790383, 21390155, 21022049, 20113003]
- Japan Science Society
- Takeda Science Foundation
- Mitsubishi Foundation
- Grants-in-Aid for Scientific Research [21390155, 20113003, 21022049, 20790383, 18790343, 21790334, 22689017] Funding Source: KAKEN
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M cells are responsible for uptake of mucosal antigens in Peyer's patches (PPs). Differentiation of M cells is thought to be induced by interactions between follicle-associated epithelium and PP cells; however, it remains elusive what types of immune cells function as M-cell inducers. Here, we attempted to identify the cells that serve as an M-cell inducer in PP. We found that a unique B-cell subset characterized by CCR6(hi)CD11c(int) resided in the subepithelial dome (SED) in mouse PP. CCR6(hi)CD11c(int) B cells showed chemotactic migration in response to CCL20. Furthermore, this unique B-cell subset substantially decreased in PP of CCR6-deficient mice, indicating that the SED localization of CCR6(hi)CD11c(int) B cells is most likely regulated by the CCL20-CCR6 system. Concomitantly, CCR6 deficiency caused remarkable decrement of M cells. Moreover, adoptive transfer of CCR6(hi)CD11c(int) B cells from wild-type mice restored the M-cell decrement in CCR6-deficient mice. Collectively, the spatial regulation of CCR6(hi)CD11c(int) B cells via the CCL20-CCR6 system may play a vital role in M-cell differentiation in mice.
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