KLRG1 (Killer Cell Lectin Like Receptor G1)

Additionally, it discusses emerging therapeutic strategies to enhance NK cell activation, such as pharmacological agents (e.g., γ-PGA, α-GalCer), innate immune agonists (e.g., STING, RIG-I), genetic engineering (e.g., CAR-NK, iPSC-NK cells), and combination therapies with immune checkpoint inhibitors or monoclonal antibodies (e.g., cetuximab)...Despite challenges like immunosuppressive tumor microenvironments and limited NK cell persistence, advancements in genetic engineering and nanoparticle delivery systems offer promising solutions. Future research should focus on integrating mechanistic insights with clinical trial design to optimize NK cell-based therapies for HPV-associated malignancies.

This discovery suggests a new mechanism for TCR involvement in irAE myocarditis, focusing on T cell activation through the TCR's functional promiscuity, which relies more on TCR-MHC interactions than on specific peptide features. Overall, this research provides a foundation for new strategies targeting TCR physical properties to reduce risks and develop more precise therapies for vulnerable patients.

This case shows phased immune rebalancing under long-term IL-17A blockade. Serial monitoring revealed dynamic exhaustion marker changes and partial regulatory recovery linked to clinical improvement, underscoring the value of longitudinal immune profiling for personalized management of complex autoimmune syndromes.

Overall, addition of DAC to the conditioning regimen was associated with favorable immunomodulatory effects on NK and T cells post-alloSCT in AML patients. These findings suggest that DAC may enhance donor NK and T cell-mediated graft-versus-tumor responses supporting its further clinical evaluation as an adjuvant prior to alloSCT.

Therapeutic benefit was dependent on CD8+ T cells and independent of NK cells and Nkg2d. Together, our study supports that IL-15C improves anti-PD-L1 in PDA through sustaining antitumor T-cell function.

Valganciclovir (VGC), as an add-on therapy in patients with disseminated Kaposi Sarcoma/human immunodeficiency virus (DKS/HIV), modulates the activation of T-cell subsets; however, its effect on the T-cell immunosenescence profile is unclear...The microenvironment generated in DKS/HIV patients increases the frequency of T-cells exhibiting an immunosenescence phenotype, and this effect is independent of the treatment schedule used, suggesting that during coinfection, a chronic immunosuppressive microenvironment may develop, impairing immune surveillance and resilience. These results could be explored to identify novel therapeutic approaches.

Flow-cytometry-based immunomonitoring showed ibrutinib's influence on inhibitory T-cell phenotypes, showing ≥25% reduction in PD1+ and PD1+ KLRG1+ CD4+-T-cells in four patients. Taken together, besides direct anti-B-cell efficacy, ibrutinib improves chemotherapy efficiency by reconstituting an effective immune system and enhancing immune cell control.

Conditional expression of Parkin induced HMGB1 release, activated intratumoral CD8+ T cells, and suppressed syngeneic tumor growth in vivo in a response that was abolished by HMGB1 silencing. These data identify that Parkin-LEV regulated release of HMGB1 reprograms antitumor immunity via stimulation of IFN signaling and expansion of specialized CD8+ T cell subsets.

Notably, during the chronic phase of the infection, pop1 cannot retain its functionality, irrespective of its origin, which may hamper its ability to control reactivation. Our observations emphasize that the differentiation of exhausted CD8 T cells in non-viral infections, like chronic toxoplasmosis, follows a different pattern than established models and highlights the need to develop new immune strategies better tailored for a broad range of pathogens.

CD8+ T cells showed decreased IFN-γ expression after PMA/BFA stimulation in EBV + DLBCL(P = 0.015). These findings suggested that EBV antigen-specific T cell functional deficits might correlate with altered T cell subset distributions, heightened levels of exhaustion and senescence, and diminished expression of immune effector molecules.

These features are coupled with a unique transcription factor landscape, including high expression of thymocyte selection associated high mobility group box (TOX) and HELIOS (IKZF2), and these signatures continue in postnatal life until at least 2 mo of age. We conclude that early-life human CD8+ T cells maintain a unique transcriptional state associated with an accelerated effector switch and short-lived effector program, revealing key nodes of regulation relevant for the unique immunobiology of neonatal humans.

In colitis, Perturb-STNet identified key genes (Csf1r, Col6a1, Lgr4, Myc, and Fzd5) and mediator pairs (Itga5-Flnc, Cd68-Csf1r, Csf1r-Cx3cl1, and Tnfrsf1b-Bmp1) involved in immune regulation, matrix remodeling, and epithelial repair, offering potential therapeutic targets. Overall, Perturb-STNet enables robust identification of spatiotemporal regulatory networks in single-cell perturbation data across diverse disease contexts.