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. 2023 Aug 6;11(8):e007180. doi: 10.1136/jitc-2023-007180

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© Author(s) (or their employer(s)) 2023. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See http://creativecommons.org/licenses/by-nc/4.0/.

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TCR signal strengths and their relation to T-cell differentiation and function. (A) Assessment of the functional avidity of nine Jurkat-TCR cells. The cells were co-cultured with autologous B-cell antigen presenting cells pulsed with different concentrations of antigenic peptides. Jurkat-TCR cells specific for CMV pp6524 were used as a high affinity TCR T-cell control. (B) Summary of the 1/logEC50 values for nine tumor antigen-specific T cells. (C) Correlations between TCR signal strengths (1/logEC50) and the mean value of z-scores for each tumor antigen-specific TCR clonotype for GOBP gene signatures related to cell signaling, cytotoxicity, proliferation, response to cytokine and cytokine production. (D) The z-scores of each clone in GOBP gene sets in C plotted according to the tumor antigen-specificity. TCR, T-cell receptor; CMV, cytomegalovirus: GOBP, Gene Ontology Biological Process.