ArticleJournal for immunotherapy of cancer2026
Integrin CD11b/CD18 reprograms macrophage polarization by suppressing ERK/STAT3 signaling to enhance antitumor immunity in colitis-associated colorectal cancer.
Article in Journal for immunotherapy of cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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12 authors.
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Abstract
backgroundChronic inflammation is a well-established driver of colorectal cancer (CRC), with the resulting inflammatory microenvironment facilitating tumor initiation and progression. The integrin CD11b/CD18, a leukocyte-specific heterodimeric adhesion receptor, mediates critical immunoregulatory functions during inflammatory responses. However, the roles and mechanisms of CD11b/CD18 in colitis-associated colorectal cancer (CAC) remain unclear.
methodsTo investigate the impact of CD11b/CD18 deficiency on colorectal carcinogenesis, an azoxymethane/dextran sodium sulfate-induced CAC model was established with CD11b and CD18 single-knockout and double-knockout mice. The tumor immune microenvironment was characterized using multicolor flow cytometry. Transcriptomic changes in tumor-associated neutrophils (TANs) and macrophages (TAMs) on CD11b/CD18 ablation were profiled by RNA sequencing. Functional crosstalk between TANs and TAMs was assessed via co-culture experiments. The direct role of CD11b/CD18 in TAM polarization and antitumor activity was evaluated using in vitro agonist assays, and the involvement of the extracellular signal-regulated kinase (ERK)/signal transducer and activator of transcription 3 (STAT3) axis was validated with pathway-specific inhibitors.
resultsBioinformatics analysis revealed significant downregulation of
conclusionsOur findings establish that integrin CD11b/CD18 orchestrates antitumor immunity by modulating the TME, particularly through direct TAM reprogramming and indirect TAN-TAM crosstalk, highlighting its potential as an immunotherapeutic target for CAC.
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