The expression of beta 2-integrins on gammadelta T cells in naïve mice or those with experimental autoimmune encephalomyelitis (EAE) remains poorly characterized. We compared beta 2-integrin expression and cytokine production between gammadelta and alphabeta T cells over the acute course of EAE. We observed that unlike in alphabeta T cells, beta 2-integrin expression on gammadelta T cells increased significantly from baseline, peaked at Day 10, and remained unchanged in the draining lymph nodes or declined in the spleen and CNS by Day 15. In addition, IFN-gamma- and TNF-alpha-producing gammadelta T cells infiltrated the CNS rapidly and produced significantly more of these cytokines than alphabeta T cells throughout the course of EAE. These results suggest unique roles for beta 2-integrins in the trafficking of gammadelta versus alphabeta T cells during EAE and that gammadelta T cells infiltrate the CNS rapidly, producing cytokines, which modulate acute disease.
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Smith et al. (2007) studied this question.
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