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. 2019 Aug 27;10:2000. doi: 10.3389/fimmu.2019.02000

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At least a portion of this work is authored by Jeffrey I. Cohen on behalf of the U.S. Government and, as regards Dr. Cohen and the U.S. Government, is not subject to copyright protection in the United States. Foreign and other copyrights may apply.

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) and the copyright owner(s) 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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Impaired T cell receptor signaling in cells from the patient with homozygous ITK mutations. (A) Impaired calcium flux in the patient compared to healthy controls following anti-CD3 crosslinking, plotted by Fluo-4 as a function of time. (B) Impaired phosphorylation of ITK in patient cells following stimulation for the indicated times with anti-CD3 antibody, compared to control cells. (C) Phosphorylation of PLCγ at various times after CD3 stimulation in patient and control. Total PLCγ served as a loading control. (D) Phosphorylation of PKC in patient cells following CD3 stimulation at various times compared to control. Actin served as a loading control. (B–D) The graphs show quantification of the blots. The experiments were repeated three times and a representative result is shown.