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. Author manuscript; available in PMC: 2012 Mar 1.
Published in final edited form as: J Immunol. 2011 Aug 3;187(5):2783–2793. doi: 10.4049/jimmunol.1100804

Figure 6. CLA+Vγ9Vδ2 T cells produce psoriasis-relevant inflammatory mediators.

Figure 6

CLA+Vγ9Vδ2 T cells from healthy controls were sorted and stimulated with HMB-PP, CD3/28 beads or PMA/Ionomycin before analyzing supernatant by multiplex bead assay. Activated CLA+Vγ9Vδ2 T cells up-regulated their IFN-γ and TNF-α production (representative experiment, n=8) (A). IL-17A production was assessed in circulating Vγ9Vδ2 T cells by flow cytometry after gating on the Vγ9 subset. A small percentage of Vγ9+ T cells produced IL-17A which was enriched in the CLA+Vγ9+ subset (B). CLA+Vγ9Vδ2 T cells produced the chemokine IL-8 as assessed by multiplex bead assay (C). The CC-chemokines CCL3, CCL4 and CCL5 were produced already constitutively. The production of CCL3 and CCL4 was increased upon activation, whereas CCL5 production could not be further up-regulated (all one representative experiment, n=11) (C) IGF-1 production was assessed by flow cytometry. Unstimulated cells cultured with medium alone showed a subtle constitutive production of IGF-1 (light grey). PMA/Ionomycin (red) and HMB-PP (dark grey) led to up-regulation of IGF-1 production in CLA+Vγ9Vδ2 T cells (D). Relative IGF-1 expression as assessed by quantitative PCR showed an up-regulation of IGF-1 expression upon activation also with IFN-α (n=4) (D).