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. Author manuscript; available in PMC: 2015 May 1.
Published in final edited form as: Immunol Rev. 2014 May;259(1):40–59. doi: 10.1111/imr.12170

Figure 3. CD18 is not required for Treg cell access to IL-2 in secondary lymphoid tissues.

Figure 3

CD4+CD25+ Treg cells were isolated from WT and Itgb2−/− (CD18-knockout) mice and adoptively transferred into congenically marked WT recipient mice. At 36 hours after transfer, pStat5 staining was performed directly ex vivo to determine the ability of endogenous Treg cells (left), recovered WT Treg cells (middle) and recovered Itgb2−/− Treg cells (right) to access paracrine IL-2 in the spleen. The average pStat5+ frequencies for these Treg cell populations are shown in the bar graph at the far right (n=3 data points per group). The CD18 integrin constitutes the beta subunit of LFA-1 (when paired with CD11a). Whereas LFA-1-dependent cellular synapses were shown to facilitate IL-2 signaling in effector T cells (see reference, these data suggest that Treg cells utilize a mechanism distinct from LFA-1 integrin interactions to access paracrine IL-2 in the T cell zones of the spleen.