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tumor-infiltrating lymphocytes

Functional Th1-Oriented T Follicular Helper Cells That Infiltrate Human Breast Cancer Promote Effective Adaptive Immunity

[Journal of Clinical Investigation] Scientists found that CD4+ Tfh TIL, CD8+ TIL and TIL-B, co-localizing in TLS, all expressed the CXCL13 receptor CXCR5.

Context-Dependent Immunomodulatory Effects of MEK Inhibition are Enhanced with T-Cell Agonist Therapy

[Cancer Immunology Research] Scientists modeled tumor-specific MEK inhibition (MEKi) through CRISPR/Cas-mediated genome editing of tumor cells and pharmacologic MEKi with cobimetinib in a RAS-driven model of colorectal cancer.

NAD+ Supplement Potentiates Tumor-Killing Function by Rescuing Defective TUB-Mediated NAMPT Transcription in Tumor-Infiltrated T Cells

[Cell Reports] By performing both whole-genome CRISPR and metabolic inhibitor screens, researchers identified that nicotinamide phosphoribosyltransferase (NAMPT) was required for T cell activation.

The CD155/TIGIT Axis Promotes and Maintains Immune Evasion in Neoantigen-Expressing Pancreatic Cancer

[Cancer Cell] Using multiple preclinical models of neoantigen-expressing pancreatic adenocarcinoma (PDAC), scientists demonstrated that intratumoral neoantigen-specific CD8+ T cells adopted multiple states of dysfunction, resembling those in tumor-infiltrating lymphocytes of PDAC patients.

Virus Induced Lymphocytes (VIL) as a Novel Viral Antigen-Specific T Cell Therapy for COVID-19 and Potential Future Pandemics

[Scientific Reports] Using a novel SARS-Cov-2-specific artificial antigen presenting cell, coupled with a rapid expansion protocol as practiced in tumor infiltrating lymphocytes therapy, researchers generated an immune catalytic quantity of VIL.

Anti-Tumor Immunity in Mismatch Repair-Deficient Colorectal Cancers Requires Type I IFN–Driven CCL5 and CXCL10

[Journal of Experimental Medicine] The authors discovered that selective recruitment and activation of systemic CD8+ T cells into DNA mismatch repair colorectal cancers strictly depend on overexpression of CCL5 and CXCL10 due to endogenous activation of cGAS/STING and type I IFN signaling by damaged DNA.

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