Correction: Precursor central memory versus effector cell fate and naïve CD4⁺ T cell heterogeneity

A pT_CM differentiation pathway arising from naïve CD4⁺ T cells(sixth paragraph)

To experimentally validate the temporal correlation between cells that have received IFN signaling and cells that end up in the TCM lineage, we generated dual reporter and fate-mapper mice by breeding the Mx1^GFP mice reporting on Mx1 transcription from the endogenous locus (Uccellini and García-Sastre, 2018) with the transgenic Mx1^Cre mice (Kühn et al., 1995) and with mice harboring a Rosa26^{lox-STOP-lox-tdTomato} recombination reporter allele, in which tdTomato (tdT) expression irreversibly tags cells that have received a type I IFN signal. Mx1^GFP × tgMx1^CreRosa26^lsl-tdT mice were infected with L.m.-gp66 and assessed for history of IFN signaling (i.e., Mx1 expression) in antigen-specific CD4⁺ T cells identified using LLO:I-A^b or gp66:I-A^b tetramers on day 7 after infection (Fig. 3 j). It is noteworthy that the Mx1 transcript was not one of the top differentially expressed genes (DEGs) within the signature ISG gene set. Therefore, Mx1^GFP expression likely faithfully reports on cells experiencing the strongest type I IFN signal as noted in the original study (Uccellini and García-Sastre, 2018) rather than reflecting low tonic signaling or potential spurious expression of some ISGs in T cells. This analysis revealed an increased frequency of Mx1 fate-mapped cells amongst CD62L⁺ pT_CM cells relative to their T_FH or T_H1 counterparts (Fig. 3, k and l), confirming the predicted trajectory identified earlier in which cells receiving type I IFN signals adopt a pT_CM fate.