Fig 5. Loss of ATMIN and NBS1 leads to intestinal inflammation due to infiltration of cytokine-producing T cells.

(A) Histological analysis by H&E staining of large intestine of control, ATM^-/-, ATMIN^ΔL, NBS1^ΔL, ATMIN^ΔLNBS1^ΔL mice at 12 weeks of age. (B) Histological scores of the large intestine of control, ATM^-/-, ATMIN^ΔL, NBS1^ΔL, ATMIN^ΔLNBS1^ΔL and 3 individual moribund ATMIN^ΔLNBS1^ΔL mice. (C) Histological analysis by anti-CD3 staining of the large intestine of control and a moribund ATMIN^ΔLNBS1^ΔL mouse. (D) Representative flow cytometry data of CD4 and CD8 expression, as well as (E) TCRβ and TCRγδ expression on isolated IELs from the small intestine of control, ATMIN^ΔL, NBS1^ΔL and ATMIN^ΔLNBS1^ΔL mice, along with the quantification of D-E. N = 5–8 mice per genotype. (F) Representative flow cytometry data of IL17A and IFNγ production by YFP^- and YFP⁺ IELs (gated on the CD4⁺ population) isolated from the small intestine of control and ATMIN^ΔLNBS1^ΔL mice after PMA and ionomycin stimulation. (G) Large intestinal sections from control, ATM^-/-, ATMIN^ΔL, NBS1^ΔL and ATMIN^ΔLNBS1^ΔL mice were stained for γH2AX and DAPI. Error bars represent SEM (**P<0.01, ***P<0.001).