γδ T cells promote anterior chamber-associated immune deviation and immune privilege through their production of IL-10

Hossam M. Ashour, Jerry Y. Niederkorn

Research output: Contribution to journalArticle

45 Citations (Scopus)

Abstract

Anterior chamber-associated immune deviation (ACAID) is a form of peripheral tolerance that is induced by introducing Ags into the anterior chamber (AC) of the eye, and is maintained by Ag-specific regulatory T cells (Tregs). ACAID regelates harmful immune responses that can lead to irreparable injury to innocent bystander cells that are incapable of regeneration. This form of immune privilege in the eye is mediated through Tregs and is a product of complex cellular interactions. These involve F4/80+ ocular APCs, B cells, NKT cells, CD4+CD25+ Tregs, and CD8+ Tregs. γδ T cells are crucial for the generation of ACAID and for corneal allograft survival However, the functions of γδ T cells in ACAID are unknown. Several hypotheses were proposed for determining the functions of γδ T cells in ACAID. The results indicate that γδ T cells do not cause direct suppression of delayed-type hypersensitivity nor do they act as tolerogenic APCs. In contrast, γδ T cells were shown to secrete IL-10 and facilitate the generation of ACAID Tregs. Moreover, the contribution of γδ T cells ACAID generation could be replaced by adding exogenous recombinant mouse IL-10 to ACAID spleen cell cultures lacking γδ T cells.

Original languageEnglish (US)
Pages (from-to)8331-8337
Number of pages7
JournalJournal of Immunology
Volume177
Issue number12
StatePublished - Dec 15 2006

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Anterior Chamber
Interleukin-10
T-Lymphocytes
Peripheral Tolerance
Natural Killer T-Cells
Delayed Hypersensitivity
Regulatory T-Lymphocytes
Allografts
Regeneration
B-Lymphocytes
Spleen
Cell Culture Techniques
Wounds and Injuries

ASJC Scopus subject areas

  • Immunology

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γδ T cells promote anterior chamber-associated immune deviation and immune privilege through their production of IL-10. / Ashour, Hossam M.; Niederkorn, Jerry Y.

In: Journal of Immunology, Vol. 177, No. 12, 15.12.2006, p. 8331-8337.

Research output: Contribution to journalArticle

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