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. 2017 Feb;214(2):269–283. doi: 10.1084/jem.20161846

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© 2017 Tangye 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.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/).

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Figure 2. — Signaling pathways responsible for generating cell-mediated EBV-specific immunity. The scheme highlights the key cell surface receptor-induced signaling pathways that, when mutated, manifest as PIDs characterized by increased susceptibility to EBV-induced disease. Genes found to be mutated in these conditions (SAP/SH12D1A, MAGT1, ITK, CD27, CD70, NFKB1, and RASGRP1) are highlighted by red boxes. XIAP is not included here, as the mechanism by which mutations in XIAP cause disease remains unknown.