Bacillus subtilis-specific poly-gamma-glutamic acid regulates development pathways of naive CD4(+) T cells through antigen-presenting cell-dependent and -independent mechanisms
- Authors
- Kim, Sunghoon; Yang, Jun Young; Lee, Kyuheon; Oh, Kyu Heon; Gi, Mia; Kim, Jung Mogg; Paik, Doo Jin; Hong, Seokmann; Youn, Jeehee
- Issue Date
- Aug-2009
- Publisher
- OXFORD UNIV PRESS
- Keywords
- antigen-presenting cells; Bacillus subtilis; poly-gamma-glutamic acid; T-h
- Citation
- INTERNATIONAL IMMUNOLOGY, v.21, no.8, pp.977 - 990
- Indexed
- SCIE
SCOPUS
- Journal Title
- INTERNATIONAL IMMUNOLOGY
- Volume
- 21
- Number
- 8
- Start Page
- 977
- End Page
- 990
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/176411
- DOI
- 10.1093/intimm/dxp065
- ISSN
- 0953-8178
- Abstract
- Peripheral naive CD4(+) T cells selectively differentiate to type 1 T-h, type 2 T-h and IL-17-producing T-h (T(h)17) cells, depending on the priming conditions. Since these subsets develop antagonistically to each other to elicit subset-specific adaptive immune responses, balance between these subsets can regulate the susceptibility to diverse immune diseases. The present study was undertaken to determine whether poly-gamma-glutamic acid (gamma-PGA), an edible and safe exopolymer that is generated by microorganisms such as Bacillus subtilis, could modulate the development pathways of T-h subsets. The presence of gamma-PGA during priming promoted the development of T(h)1 and T(h)17 cells but inhibited development of T(h)2 cells. gamma-PGA up-regulated the expression of T-bet and ROR-gamma t, the master genes of T(h)1 and T(h)17 cells, respectively, whereas down-regulating the level of GATA-3, the master gene of T(h)2 cells. gamma-PGA induced the expression of IL-12p40, CD80 and CD86 in dendritic cells (DC) and macrophages in a Toll-like receptor-4-dependent manner, and the effect of gamma-PGA on T(h)1/T(h)2 development was dependent on the presence of antigen-presenting cells (APC). Furthermore, gamma-PGA-stimulated DC favored the polarization of naive CD4(+) T cells toward T(h)1 cells rather than T(h)2 cells. In contrast, gamma-PGA affected T(h)17 cell development, regardless of the presence or absence of APC. Thus, these data demonstrate that gamma-PGA has the potential to regulate the development pathways of naive CD4(+) T cells through APC-dependent and -independent mechanisms and to be applicable to treating T(h)2-dominated diseases.
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