Notch1 and Notch 2 receptors deliver nonredundant pathogenic signals in T cells during BO-cGVHD. B10.BR recipients were conditioned with irradiation and cyclophosphamide and transplanted with B6 WT TCD BM cells (10⁷) supplemented with 80 × 10³ B6 WT, Cd4-Cre × Notch1^f/f (N1Ko), Cd4-Cre × Notch2^f/f (N2Ko), and Cd4-Cre×Notch1^f/fNotch2^f/f (N1Ko/N2Ko) T cells. (A) Notch1 and Notch2 receptors are nonredundant in driving pathogenic Notch signaling in T cells to cause BO-cGVHD. Pulmonary function tests at day 49 showing preservation of pulmonary functions in mice receiving Notch1-deficient, Notch2-deficient, or Notch1/2-deficient vs WT T cells. *P < .05 (1-way ANOVA). (B-C) Notch1 and/or Notch2 loss in T cells decreases the accumulation of GC B-cell (B) and Tfh cell (C) posttransplant in spleens of recipient animals. Spleens were harvested on day 60 posttransplant and analyzed for GC B cells as well as Tfh and Tfr cells. The Tfr/Tfh ratio was calculated by dividing the percentages of respective subsets in parental populations. *P < .05 (1-way ANOVA).