Ppp1r18 ^−/− mice are viable with impaired T cell integrin activation. (A) Generation of Ppp1r18^−/− mice. Two sgRNAs targeting the exon1 downstream of methionine residue 429, which drives the expression of α-Ptsn, were used in combination with a single-stranded DNA (ssDNA) oligonucleotide to introduce seven stop codons. (B and C)Ppp1r18^−/− mice exhibit leukocytosis. (B) Peripheral blood cell counts of WT or Ppp1r18^−/− mice. Mean ± SEM are plotted. Two-tailed t test; **, P < 0.01; ***, P < 0.001. (C) Abundance of T and B cells in MLN, PLN, and spleen (SPL) from WT or Ppp1r18^−/− mice. Data are normalized to Ppp1r18^+/+ samples = 100. Bar graphs represent mean ± SEM (n = 4 mice). Two-tailed t test; *, P < 0.05; **, P < 0.01; ***, P < 0.001. (D–G) Loss of Ptsn reduces T and B cell adhesion. CD4⁺ T cells (D–F) or B cells (G) were isolated from the spleen of WT or Ppp1r18^−/− mice. Cell adhesion to immobilized ICAM-1, VCAM-1, or MAdCAM-1 was assayed in flow condition upon stimulation with SDF-1α. Rest, no stimulation. Bar graphs represent mean ± SEM (n = 5 mice). Two-tailed t test; *, P < 0.05; **, P < 0.01; ***, P < 0.001.