Work

Absence of BCAP in myeloid cells abrogates M2 macrophage differentiation and promotes anti-tumor immunity

Year: 2025

Type: article

Abstract: . Mechanistically, BCAP enables IL-4-driven PI3K-Akt activation by mediating interactions between p85 and Grb2 without impacting STAT6 function. Strikingly, loss of BCAP, either globally or in myeloid cells, leads to suppressed tumor growth and a shift in tumor-associated macrophages toward a pro-inflammatory state and less exhausted tumor-infiltrating CD8 T cells. These findings present BCAP as a promising therapeutic target for enhancing anti-tumor immunity.

Source: iScience

DOI: 10.1016/j.isci.2025.113723

Authors: Kiana Kawarizadeh, Charles N. Vallez, Sepideh Aliyazdi, Kathrynne A. Warrick, Cierra Carafice, Irene Saha, Chandrashekhar Pasare

Institutions: Cincinnati Children's Hospital Medical Center, University of Cincinnati

Language: English

Topic: Immune cells in cancer

Subfield: Immunology

Field: Immunology and Microbiology

Domain: Life Sciences

SDG: Good health and well-being

Open Access status: gold

Estimated APC paid: $3,240

Funders: American Heart Association, National Institutes of Health, National Institute of Allergy and Infectious Diseases

Awards: G1456376370, Defining Mechanisms of T Cell-Mediated Pathology in Immune Checkpoint Inhibitor-Induced Myocarditis, Innate mechanisms of regulation of Th17 responses

OpenAlex ID: W4414919601

FWCI: 0.295

Cites: 72

Cited by: 1

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