| Literature DB >> 18566396 |
Laura Cook1, Nobuaki Miyahara, Niyun Jin, J M Wands, Christian Taube, Christina L Roark, Terry A Potter, Erwin W Gelfand, Rebecca L O'Brien, Willi K Born.
Abstract
Airway hyperresponsiveness (AHR), a hallmark of asthma and several other diseases, can be modulated by gammadelta T cells. In mice sensitized and challenged with OVA, AHR depends on allergen-specific alphabeta T cells; but Vgamma1+ gammadelta T cells spontaneously enhance AHR, whereas Vgamma4+ gammadelta T cells, after being induced by airway challenge, suppress AHR. The activity of these gammadelta T cell modulators is allergen nonspecific, and how they develop is unclear. We now show that CD8 is essential for the development of both the AHR suppressor and enhancer gammadelta T cells, although neither type needs to express CD8 itself. Both cell types encounter CD8-expressing non-T cells in the spleen, and their functional development in an otherwise CD8-negative environment can be restored with transferred spleen cell preparations containing CD8+ dendritic cells (DCs), but not CD8+ T cells or CD8- DCs. Our findings suggest that CD8+ DCs in the lymphoid tissues enable an early step in the development of gammadelta T cells through direct cell contact. DC-expressed CD8 might take part in this interaction.Entities:
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Year: 2008 PMID: 18566396 PMCID: PMC2493442 DOI: 10.4049/jimmunol.181.1.309
Source DB: PubMed Journal: J Immunol ISSN: 0022-1767 Impact factor: 5.422