How Notch and Wnt make T-cells tick

The Notch signaling pathway is a master regulator of CD8+ T cell exhaustion and differentiation during chronic infection

It is shown that the absence of Notch signal causes severe CD8+ T cell exhaustion during chronic LCMV infection and demonstrated that Notch signaling is essential to promote the differentiation of Tex progenitors into Tex effector-like cells.

Rational Engineering of Notch1 Signaling to Boost the Proliferation of CD19-BBζ CAR-T.

A critical role of Notch1 in CAR-T effector function is demonstrated and a novel strategy to augment endogenous Notch1 activity by leveraging native gene regulation is provided to augment endogenous Notch1 activity by leveraging native gene regulation.

Antigen-specific regulatory T cells eliminate cognate CD4 effector T cells through perforin, granzyme B, and Bim.

T cells (Tregs) maintain immune tolerance, yet how they selectively eliminate cognate CD4+ effector T cells remains unclear. We propose a co-activation-dependent elimination mechanism, conceptually akin to synthetic lethality. Using in vitro co-cultures, we show that simultaneous peptide-MHC II recognition by Tregs and...

CRITICAL ROLE OF BIM IN T CELL RECEPTOR RESTIMULATION-INDUCED DEATH

CD4+ cytotoxic T cells: context-dependent effectors in health and disease

Cytotoxic CD4 + T cells (CD4 + CTLs) have been identified as a specialized effector population characterized by potent cytotoxic machinery, including granzymes, perforin, and the Fas/FasL pathway, that enables the direct killing of MHC-II-expressing target cells. In addition to their classical helper function,...

Abstract IA005: Determinants of B cell fate and function in cancer

Effector B cell responses in solid malignancies are associated favorable response to immunotherapy. B cells can amplify anti-tumor immune responses via antibody production, antigen presentation, and pro-inflammatory cytokine release; yet B cells in cancer patients and tumor-bearing mice often fail to support these fu...