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. 2009 Apr 13;206(4):877–892. doi: 10.1084/jem.20082900

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© 2009 Maldonado et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jem.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

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Figure 8. — Model of receptor exclusion from the IS. (top) IFNGR, TCR, Stat, phospho-STAT1, JAK3, and eventually the common γ chain (γc) colocalize after TCR signaling. Under these conditions, inhibitors could mediate the exclusion of IL4R from the IS. (middle) IL-4 signaling blocks the recruitment of IFNGR, STAT1, and phospho-STAT1 to the TCR-rich regions of the membrane. This phenomenon could be mediated by association of inhibitors to the IFNGR and/or recruitment of γc-JAK3 to the IL4R complex. Bottom panel. In the absence of pro-Th1 molecules, IFNGR, or STAT1, the IL4R is licensed to enter the IS to induce Th2 differentiation.