Lack of protective effect of CCR3 blockade during experimental colitis may be related to CCR3 expression by colonic Tregs

Ferhat, Maroua; Hablot, Julie; Taieb, Mahdia; Salem, Fatouma; Netter, Patrick; Peyrin–Biroulet, Laurent; Jouzeau, Jean‐Yves; Moulin, David

doi:10.1002/ctm2.455

Cited by 3 publications

(1 citation statement)

References 10 publications

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“… 47 Ccr 3 is expressed by CD4 Tregs specifically among T cells. 49 It is known that hypoxia increases the production of CCR3 ligands 50 and that CD4 Tregs selectively accumulate in hypoxic areas. 51 Interestingly, Ccr3 was the most expressed gene in Foxp3UP CD8 TILs, and CCR3 remained upregulated in these cells even in the late phase of ACT.…”

Section: Discussionmentioning

confidence: 99%

FOXP3 expression diversifies the metabolic capacity and enhances the efficacy of CD8 T cells in adoptive immunotherapy of melanoma

et al. 2023

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Section: Discussionmentioning

confidence: 99%

FOXP3 expression diversifies the metabolic capacity and enhances the efficacy of CD8 T cells in adoptive immunotherapy of melanoma

et al. 2023

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CCL11 exacerbates colitis and inflammation-associated colon tumorigenesis

et al. 2021

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Eosinophil Depletion as a Potential Therapeutic Strategy in Acute and Chronic Intestinal Inflammation Based on a Dextran Sulfate Sodium Colitis Model

Jacobs,

Deleu,

Cremer

et al. 2024

Inflammatory Bowel Diseases

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Background A role for eosinophils in intestinal inflammation and fibrosis in the context of inflammatory bowel disease has been suggested, yet the precise nature, whether causal or secondary remains debated. Hence, it remains unclear whether targeting eosinophils should be further explored as a treatment option in inflammatory bowel disease. Methods Acute and chronic dextran sulfate sodium colitis was induced in wild-type C57BL/6 mice. Eosinophils were depleted by anti-CCR3 injections before colitis induction in a chronic model and after colitis onset in an acute model in order to investigate the impact of eosinophil depletion on pre-existing colitis. Inflammation was assessed using the disease activity index, macroscopic damage, and histological disease activity score. In the chronic model, fibrosis was assessed by examining colon weight/length ratio, collagen deposition through Martius Scarlet Blue staining, hydroxyproline assay, and COL1A1 expression. Protein and gene expression were assessed using the Meso Scale Discovery platform and real-time quantitative polymerase chain reaction. Results In the acute and chronic colitis model, eosinophil depletion resulted in reduced disease activity and faster recovery, as observed via the total area under the curve of the disease activity index (P = .004 and P = .02, respectively), macroscopic damage score (P = .009 and P = .08, respectively), and histological disease activity score (P = .09 and P = .002, respectively). In the acute model, the accelerated recovery was accompanied by an increase in interleukin (IL)-10 (P = .03) and a decrease in IL-4 (P = .03) and IL-6 (P = .009). Colon weight/length ratio and collagen deposition were not affected by eosinophil depletion. Conclusions Eosinophil depletion prevents and decreases intestinal inflammation in a preclinical dextran sulfate sodium model without affecting fibrosis. These results pave the way for exploring eosinophil depletion as a novel treatment modality in addressing intestinal inflammation.

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Lack of protective effect of CCR3 blockade during experimental colitis may be related to CCR3 expression by colonic Tregs

Cited by 3 publications

References 10 publications

FOXP3 expression diversifies the metabolic capacity and enhances the efficacy of CD8 T cells in adoptive immunotherapy of melanoma

FOXP3 expression diversifies the metabolic capacity and enhances the efficacy of CD8 T cells in adoptive immunotherapy of melanoma

CCL11 exacerbates colitis and inflammation-associated colon tumorigenesis

Eosinophil Depletion as a Potential Therapeutic Strategy in Acute and Chronic Intestinal Inflammation Based on a Dextran Sulfate Sodium Colitis Model

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