Didem Ağaç Çobanoğlu

Shigellosis is a highly contagious and severe gastrointestinal infection caused by bacteria of the genus Shigella. Whereas exposure to a small number of Shigella bacteria can cause disease in humans, mice are naturally resistant. However, mice deficient in the NAIP–NLRC4 inflammasome and caspase-11 (Nlrc4−/−Casp11−/− mice) have recently emerged as a genetically tractable model to study human shigellosis.

Cues from the local microenvironment influence the differentiation state of T cells, resulting in a diverse array of functions. Transcription factors (TFs) control the differentiation of cells; understanding how and which TFs regulate CD8+ T cell differentiation could improve the outcome of CD8+ T cell-based therapies and help to uncover yet-unknown biology behind fundamental processes. In this preprint (not peer reviewed), Chung et al.

Abstract Immune checkpoint therapies (ICT) improve overall survival of patients with cancer but may cause immune-related adverse events (irAEs) such as myocarditis. Cytotoxic T lymphocyte-associated antigen 4 immunoglobulin fusion protein (CTLA-4 Ig), an inhibitor of T cell costimulation through CD28, reverses irAEs in animal models. However, concerns exist about potentially compromising antitumor response of ICT.