bims-maitce 2026-01-11 papers

Issue of 2026–01–11
three papers selected by
Andy E. Hogan, Maynooth University

Biochim Biophys Acta Mol Basis Dis. 2026 Jan 03. pii: S0925-4439(25)00501-0. [Epub ahead of print]1872(3): 168151

MAIT cells accumulated via CXCL12-CXCR4 chemotaxis are involved in pathologic gastric inflammation among Helicobacter pylori-infected patients.

Fang Zhang, Youjian Zhou, Tingting Xia, Yue Xu, Taojun He, Bin Li, Shasha Yang, Ying Chen, Honglei Chen, Chao Wu.

BACKGROUND: Helicobacter pylori can cause gastritis, peptic ulcers, and even gastric cancer. In addition to conventional T cells, mucosal-associated invariant T (MAIT) cells may have an important immunologic role in mucosal infectious diseases. However, the phenotypic and effector characteristics of gastric MAIT cells and the relationship between mucosal MAIT cells and H. pylori-related diseases have not been established.
METHODS: We analyzed the phenotypes and cytokines of gastric and peripheral MAIT cells from H. pylori-infected patients by flow cytometry. CXCL12-mediated chemotaxis of MAIT cells was measured by Transwell assay. Relationship between MAIT cells and inflammation of H. pylori-infected gastric diseases was assessed with immunofluorescence staining and histopathological score.
RESULTS: The number of gastric MAIT cells was significantly increased but the frequency of peripheral MAIT cells were decreased in patients with H. pylori infections. The gastric MAIT cells were activated with high expression of CD69 and CD38, and produced several pro-inflammatory cytokines. Furthermore, we observed the expression of CXCR4 and CXCL12 were upregulated in H. pylori-infected stomachs. CXCL12 promoted MAIT cells to migrate, which was blocked by a CXCR4 antagonist. Finally, we demonstrated that the number of gastric MAIT cells was positively correlated with severe inflammation in H. pylori-infected stomachs.
CONCLUSIONS: Gastric MAIT cells were accumulated and activated in H. pylori-infected stomachs, which may be involved in the pathologic inflammation of H. pylori-related gastric diseases.

Keywords: CXCR4; Chemotaxis; H. pylori; Mucosal-associated invariant T cells; Pathologic inflammation

DOI: https://doi.org/10.1016/j.bbadis.2025.168151

Cells. 2025 Dec 31. pii: 69. [Epub ahead of print]15(1):

MAIT Cells in Liver Disease.

Adiba I Azad, Florencia Gutierrez, Gregory J Gores.

Mucosal-associated invariant T (MAIT) cells are abundant innate-like T lymphocytes in the human liver which can provide antimicrobial defense, amplify inflammatory processes and mediate tissue repair and fibrosis depending on microenvironmental cues. Chronic liver diseases of diverse etiologies, including viral hepatitis, metabolic dysfunction-associated steatotic liver disease, alcohol-associated liver disease, biliary tract disease, autoimmune hepatitis and hepatocellular carcinoma are accompanied by numerical and functional adjustments in the MAIT cell population. In this review, we integrate existing data on MAIT cell markers and functions in diverse liver diseases, comparing how these cells are similarly or differentially shaped by distinct pathogenic contexts. Finally, we propose a spatially anchored conceptual and technical framework to study MAIT cell biology in liver disease.

Keywords: alcohol-associated liver disease; chronic liver disease; liver fibrosis; metabolic dysfunction-associated steatotic liver disease; mucosal-associated invariant T (MAIT) cells; primary sclerosing cholangitis; unconventional T cells; viral hepatitis

DOI: https://doi.org/10.3390/cells15010069

Mol Biol Rep. 2026 Jan 06. 53(1): 254

Redefining cell therapy: CAR-engineered innate immune cells to conquer solid and hematologic malignancies.

Ashik Anil Mathew, Ronak Raheja, Kannan Ramalingam.

Chimeric antigen receptor (CAR) technology has revolutionized cancer therapy, yet its full potential remains untapped within the innate immune system. Beyond CAR-T cells, a growing cadre of MHC-independent effectors, including NK cells, macrophages, γδ T cells and the emerging innate-like T cells such as invariant NKT (iNKT) and mucosal-associated invariant T (MAIT) cells, offer complementary mechanisms for tumor recognition and elimination. These platforms combine facile, off-the-shelf manufacture from healthy donors with low graft-versus-host disease risk and a reduced propensity for severe cytokine release syndromes. Mechanistically, they span missing-self and antibody-dependent cytotoxicity (NK), phagocytosis and cross-presentation (macrophages), stress-ligand recognition (γδ T cells), and rapid, tissue-tropic, TCR-mediated responses to conserved lipid and metabolite antigens (iNKT via CD1d; MAIT via MR1). CAR engineering of these cells leverages their innate rapidity, innate/adaptive cross-talk, and distinctive homing to confront heterogeneous and immune-evasive tumors. Here, we synthesize recent advances in cell design, dual/split CARs, switchable control systems, armored payloads and synthetic-biology circuits, and evaluate translational progress, manufacturing bottlenecks, and regulatory considerations. We argue that integrating innate and innate-like programs with precision CAR architectures will yield a new generation of universal, resilient cellular therapeutics with broadened antigen reach, improved safety profiles, and enhanced capacity to overcome the suppressive tumor microenvironment.

Keywords: CAR-Innate cells; CAR-NK; CAR-macrophage; CAR-γδ t cells; Chimeric antigen receptor; Solid tumors

DOI: https://doi.org/10.1007/s11033-025-11407-0