Journal
GLYCOBIOLOGY
Volume 28, Issue 1, Pages 50-58Publisher
OXFORD UNIV PRESS INC
DOI: 10.1093/glycob/cwx093
Keywords
asthma; IL-10; microbiota; polysaccharide; T cell
Categories
Funding
- American Asthma Foundation [10-0187]
- National Institutes of Health [F32-AI114109, T32-AI007024, DP2-OD004225, R01-GM082916]
- Hartwell Foundation
Ask authors/readers for more resources
Inhibition of peripheral inflammatory disease by carbohydrate antigens derived from normal gut microbiota has been demonstrated for the GI tract, brain, peritoneum, and most recently the airway. We have demonstrated that polysaccharide A (PSA) from the commensal organism Bacteroides fragilis activates CD4(+) T cells upon presentation by the class II major histocompatibility complex, and that these PSA-experienced T cells prevent the development of lung inflammation in murine models. While the PSA-responding T cells themselves are not canonical FoxP3(+) regulatory T cells (Tregs), their ability to prevent inflammation is dependent upon the suppressive cytokine IL-10. Using an adoptive T cell transfer approach, we have discovered that PSA-experienced T cells require IL-10 expression by PSA-naive recipient animals in order to prevent inflammation. A cooperative relationship was found between PSA-activated effector/memory T cells and tissue-resident FoxP3(+) Tregs both in vivo and in vitro, and it is this cooperation that enables the suppressive activity of PSA outside of the gut environment where exposure takes place. These findings suggest that carbohydrate antigens from the normal microbiota communicate with peripheral tissues to maintain homeostasis through T cell-to-T cell cooperation.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available