Figure S4.
Absence of IFN-I and IFN-II signaling promotes TSCMcell differentiation during acute LCMV Armstrong infection. Related to Figs. 7 and 8. (A) Total lymph node IFNγ+ of indicated cells from control-treated and d0–1 IFNAR-blocked mice at d4 of acute LCMV Armstrong infection. (B) Expression of Cxcl9-RFP and Cxcl10-BFP in cDC1, cDC2, and moDC populations from REX3 hosts crossed to indicated IFN-deficient mice. (C) Images from Fig. 7 E. LSFM micrographs of intact wild-type, Ifnar−/−, Ifng−/−, and 2xIFN−/− mouse REX3 lymph nodes. Images are 200-µm longitudinal slices through the lymph node center. Scale bars represent 100 µm. The dashed line indicates the lymph node outline. Pseudocolor FIRE LUT heat maps for each REX3 reporter. Images are representative of three individual experiments with at least three mice in each group in each experiment. (D) Total P14 cell number in each wild-type or IFN-deficient host mouse. (E) Representative plots of P14 cells showing TEFF (KLRG1+SLAMF6−), TSCM (KLRG1−SLAMF6+), and TEX (KLRG1−SLAMF6−) cells. (F) Model of IFN control of chemokine production and CD8+ T cell position within lymph nodes and how this correlates with in vitro migration assay chemokine concentration. Lymph nodes indicate P14 cell location and chemokine receptor expression in Ifng−/− and 2xIFN−/− (left), wild-type (middle), and Ifnar−/− and d0–1 IFNAR-blocked (right) settings. Dotted lines indicate correlation to chemokine concentration and the bell curve of the cell migration index in in vitro assays. The wild-type setting correlates with optimal CXCL9 (red) and CXCL10 (blue) gradient formation to facilitate the generation of both TEFF (green) and TSCM (purple) cells. Ifng−/− and 2xIFN−/− settings exhibit low CXCL9 and CXCL10 expression to promote cell retention in the paracortex, increasing the generation of TSCM cells and reducing TEFF cells. In Ifnar−/− and d0–1 IFNAR-blocked settings, increased CXCL9 and CXCL10 expression causes downregulation of surface CXCR3, preventing cell migration and increased TSCM cell and reduced TEFF cell differentiation. Each dot in A, B, and D represents a single sample. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.

Absence of IFN-I and IFN-II signaling promotes T SCM cell differentiation during acute LCMV Armstrong infection. Related to Figs. 7 and 8. (A) Total lymph node IFNγ+ of indicated cells from control-treated and d0–1 IFNAR-blocked mice at d4 of acute LCMV Armstrong infection. (B) Expression of Cxcl9-RFP and Cxcl10-BFP in cDC1, cDC2, and moDC populations from REX3 hosts crossed to indicated IFN-deficient mice. (C) Images from Fig. 7 E. LSFM micrographs of intact wild-type, Ifnar−/−, Ifng−/−, and 2xIFN−/− mouse REX3 lymph nodes. Images are 200-µm longitudinal slices through the lymph node center. Scale bars represent 100 µm. The dashed line indicates the lymph node outline. Pseudocolor FIRE LUT heat maps for each REX3 reporter. Images are representative of three individual experiments with at least three mice in each group in each experiment. (D) Total P14 cell number in each wild-type or IFN-deficient host mouse. (E) Representative plots of P14 cells showing TEFF (KLRG1+SLAMF6−), TSCM (KLRG1−SLAMF6+), and TEX (KLRG1−SLAMF6−) cells. (F) Model of IFN control of chemokine production and CD8+ T cell position within lymph nodes and how this correlates with in vitro migration assay chemokine concentration. Lymph nodes indicate P14 cell location and chemokine receptor expression in Ifng−/− and 2xIFN−/− (left), wild-type (middle), and Ifnar−/− and d0–1 IFNAR-blocked (right) settings. Dotted lines indicate correlation to chemokine concentration and the bell curve of the cell migration index in in vitro assays. The wild-type setting correlates with optimal CXCL9 (red) and CXCL10 (blue) gradient formation to facilitate the generation of both TEFF (green) and TSCM (purple) cells. Ifng−/− and 2xIFN−/− settings exhibit low CXCL9 and CXCL10 expression to promote cell retention in the paracortex, increasing the generation of TSCM cells and reducing TEFF cells. In Ifnar−/− and d0–1 IFNAR-blocked settings, increased CXCL9 and CXCL10 expression causes downregulation of surface CXCR3, preventing cell migration and increased TSCM cell and reduced TEFF cell differentiation. Each dot in A, B, and D represents a single sample. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.

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