Anti-IFNG monoclonal antibody, clone YNH2.3 [Pacific Blue™]

Interferon Gamma Receptor (IFNGR) genes play an important role in the immune response against mycobacteria by regulating the proinflammatory cytokine Interferon Gamma (IFNG) along with subsequent mycobactericidal milieu and are potential strong candidates for investigating genetic basis of disease resistance. Present investigation was aimed at exploring the association of one SNP in IFNGR1 gene and two SNPs in IFNGR2 gene with susceptibility/resistance against bovine tuberculosis infection in cattle. All the three SNPs under investigation (rs109049057, rs109579937 and rs110689128) revealed polymorphism. SNP loci rs109049057 was found to be significantly (P < 0.01) associated with susceptibility to bovine tuberculosis in cattle in our case control population. The SNP was non-synonymous, suggesting its functional role in the immune response against bovine tuberculosis.

Tumor-infiltrating CD8+ T cells (TIL) are of the utmost importance in anti-tumor immunity. CD103 defines tumor-resident memory T cells (T-RM cells) associated with improved survival and response to immune checkpoint blockade (ICB) across human tumors. Co-expression of CD39 and CD103 marks tumor-specific T-RM with enhanced cytolytic potential, suggesting that CD39+CD103+ T-RM could be a suitable biomarker for immunotherapy. However, little is known about the transcriptional activity of T-RM cells in situ. We analyzed CD39+CD103+ T-RM cells sorted from human high-grade endometrial cancers (n = 3) using mRNA sequencing. Cells remained untreated or were incubated with PMA/ionomycin (activation), actinomycin D (a platinum-like chemotherapeutic that inhibits transcription), or a combination of the two. Resting CD39+CD103+ T-RM cells were transcriptionally active and expressed a characteristic T-RM signature. Activated CD39+CD103+ T-RM cells differentially expressed PLEK, TWNK, and FOS, and cytokine genes IFNG, TNF, IL2, CSF2 (GM-CSF), and IL21. Findings were confirmed using qPCR and cytokine production was validated by flow cytometry of cytotoxic TIL. We studied transcript stability and found that PMA-responsive genes and mitochondrial genes were particularly stable. In conclusion, CD39+CD103+ T-RM cells are transcriptionally active T-RM cells with a polyfunctional, reactivation-responsive repertoire. Secondly, we hypothesize that differential regulation of transcript stability potentiates rapid responses upon T-RM reactivation in tumors.