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. 2021 Dec 13;6:412. doi: 10.1038/s41392-021-00823-w

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — In resting T cells, CD3ζ and CD3ε remain membrane-embedded. Perhaps membrane-bound CD3ζ might be released to the cytosol, where free LCK induces tyrosine phosphorylation on at least two sites in ITAMs. This basal tyrosine phosphorylation creates docking sites for ZAP-70 interaction. After antigen engagement, the TCR complex recruits coreceptor-bound LCK that phosphorylates ZAP-70 and interacts with it through the SH2 domain facilitating tyrosine phosphorylation on other residues on ITAMs.