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. 2017 Nov 21;7:481. doi: 10.3389/fcimb.2017.00481

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Copyright © 2017 Carpino, Naseem, Frank and Konopka.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Predicted functions of Jnk1, Cbl-b, and Sts-1/2 in cell signaling. Model for how loss of function of Jnk1, Cbl-b, or the Sts proteins promotes resistance to C. albicans. The right side shows a diagram of signaling pathways in phagocytic cells of the innate immune system. Jnk1 negatively regulates the NFATc1 transcription factor to suppress expression of Fcer2a (CD23). CD23 activation induces expression of Nos2 (iNOS). Cbl-b is an E3 ligase that regulates the ubiquitination of Dectin receptors (Dectin-1,−2,−3) and the Syk protein kinase, thereby regulating their levels of expression. In T cells Sts-1 and −2 are phosphatases that counteract the activation of the kinase Zap-70 downstream of TCR engagement (left side). Syk is a homolog of Zap-70 expressed in phagocytes, suggesting the Sts proteins could negatively regulate Syk activity.