γδ T cells exacerbate intestinal fibrosis in mice with experimental colitis via activation of the CD73-adenosine receptor-cyclic AMP signaling pathway

Figure 1 Depletion of γδ T cells prevented intestinal fibrosis. A: Experimental scheme of 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced intestinal fibrosis model. γδ T cells were depleted using GL3 antibody before TNBS administration; B: TCR staining of the colon tissues after GL3 antibody administration; C: Body weight changes in the mice administrated with TNBS or TNBS + GL3 during the whole experimental period (n = 5); D: Disease activity index score evaluated in the mice administrated with TNBS or TNBS + GL3 (n = 5); E: The representative image for hematoxylin and eosin and Masson staining of colon in each group. Orange arrow indicated areas of immune cell infiltration. Scale bars: 100 μm; F: The concentrations of hydroxyproline levels in the serum of each group at week 14 (n = 3); G: The levels of hyaluronic acid, type IV collagen, laminin, and procollagen III in each group at week 14 (n = 3). Data were presented as mean ± SD. ^bP < 0.01, ^cP < 0.001. TNBS: 2,4,6-trinitrobenzenesulfonic acid; DAI: Disease activity index; H&E: Hematoxylin and eosin; HA: Hyaluronic acid; IV-C: Type IV collagen; LN: Laminin; PCIII: Procollagen III.