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. Author manuscript; available in PMC: 2018 Jul 30.
Published in final edited form as: Annu Rev Immunol. 2012 Jan 6;30:531–564. doi: 10.1146/annurev.immunol.25.022106.141623

Figure 1.

Figure 1

TCR signal strength instructs CD4+ thymocyte fate and regulatory T cell differentiation. Immature CD4 single-positive (SP) thymocytes receive TCR signals of varied strength via interactions with peptide-MHC on antigen-presenting cells. The strength of TCR signals (or functional avidity, based on a composite of individual peptide-MHC-TCR interaction affinity and peptide-MHC abundance) and their duration determines CD4 SP thymocyte fate. Upon reception of a TCR signal of high strength, most CD4 SP thymocytes undergo programmed cell death. A number of CD4 SP thymocytes receiving TCR signals of intermediate strength are able to escape deletion and are enriched for cells that are instructed to differentiate into Foxp3+ Treg cells. Weight of arrows reflects relative probability of the indicated outcomes.