E. Abu-Shah

The paper analyzes single-cell immune multi-omics data from PDAC to identify differential immunosuppressive mechanisms in distinct tumour microenvironments.

This study introduces a stochastic model of T cell activation showing that information from TCR-pMHC interactions, not binding strength, drives immune responses and suggests optimizing stochasticity could improve therapeutics.

This paper develops artificial antigen presenting cells (aAPCs) to detect and desensitize autoreactive T cells in type 1 diabetes, showing effectiveness in human and mouse models.

This study measures TCR discriminatory power against pMHC antigens and finds it is imperfect, with T cells responding to low-affinity self pMHC with KD ~1 mM.

The paper measures ultra-low TCR/pMHC affinities and finds T cells have low discriminatory power, requiring large affinity differences to trigger responses.

This study identifies immune cell states in pancreatic cancer, showing regulatory T-cells and dysfunctional CD8+ T-cells contribute to a suppressive microenvironment, suggesting new therapeutic targets.

The paper shows that different effector responses of human CD8+ T cells share a common antigen threshold across varying affinities and co-stimulatory conditions.

This paper develops a tissue-like platform to study interactions between engineered quiescent human T-cells and dendritic cells, demonstrating CD4 help and PD-1 checkpoint blockade effects.

The paper shows CD2 expression levels determine immunological synapse structure and T-cell activation by influencing CD2-CD58 localization and Src-family kinase recruitment.

The paper shows human memory CD8 T cells have higher synapse propensity than naive cells, giving them competitive advantage in immune responses.