Antigen-dependent reexpression of α4β7 by spleen-derived transgenic and endogenous memory CD8 T cells upon infection with virus or bacteria. (A–D) Splenocytes isolated from P14 immune chimeras (>30 d after LCMV Arm infection) were transferred to naive recipients. (A and B) The next day, recipients were challenged with high-dose LCMV Arm or left unchallenged. (A) α4β7 expression was monitored in blood among donor P14 (Thy1.1⁺/gp33 tetramer⁺), nontransgenic gp33-specific cells (Thy1.1⁻/gp33 tetramer⁺), and CD44^lo (naive) CD8 T cells. Representative flow cytometry data are shown. (B) Change in GMFI of α4β7 expression relative to α4β7 GMFI of memory P14 transferred to unchallenged mice that were analyzed on the same day. (C and D) As in A and B, except mice were challenged with LCMV Cl⁻13 (C) or LM-gp33 (D), or the noncognate antigen bearing inflammation control LM-WT. (E) 19 d after infection, small intestine IEL of these mice were examined for the presence of donor P14. (F) Splenocytes from LCMV Arm–immune C57BL/6J mice (which did not contain P14) were transferred to naive CD45.1 recipients. Recipients were challenged the next day with LM-gp33, and α4β7 expression among CD45.1⁻ gp33-tetramer⁺ CD8 T cells was monitored in blood. At least three mice were analyzed at each time point in each experiment. Error bars indicate SEM. One of two experiments with similar results is shown.