(A) Illustration of the huDCIR-KI mice generation. (B) Flow cytometry of huDCIR expressed in pooled BM spleen, or blood CD11b⁺ cells from WT or homogenous huDCIR-KI mice (HO). (C–E) Flow cytometry of huDCIR and tdTomato expressed in the monocytes (CD11b⁺Ly6G^–), neutrophils (CD1b⁺Ly6G⁺), and DCIR⁺ and DCIR^– cells from the BM of WT or homogenous huDCIR-KI mice. (F) Design of the peritonitis model induced by i.p. injection of 0.5 mL 2 mg/mL ZymD. (G) Flow cytometry quantitation of huDCIR-expressing (tdTomato⁺) cells in the CD45⁺ leukocytes isolated from the peritoneal lavage of WT and homogenous huDCIR-KI mice in the peritonitis model as described in F. Means ± SEM are shown, and statistical analysis is determined by 1-way ANOVA test with Dunnett’s correction compared with the PBS treated huDCIR-KI group. *P < 0.05, ***P < 0.001. (H) Design of the DSS-colitis model. Mice were fed 3% DSS in drinking water for 7 days. For the vessel staining, mice were i.v. administrated with 100 μL of 1 mg/mL 10 kDa AF680 dextran 2 days before feeding DSS water. For the DCIR⁺ cells detection, AF488 anti-DCIR mAb were i.v. injected into the mice 3 days before and 6 days after DSS feeding. CLE analyses were performed on day 0 (naive) and day 7 (colitis) during the DSS-feeding phase. (I) Representative CLE of naïve mice and mice with colitis as described in F. DCIR⁺ cells in the colonic crypts were stained with AF488 anti-DCIR mAb (green), and blood vessels running along the crypt wall were stained with AF680 dextran (red). Scale bars: 20 μm.