John rizk

The cIAP ubiquitin ligases sustain type 3 γδ T cells and ILC during aging to promote barrier immunity

Type I interferon supports γδ T‐cell homeostasis and immunity through direct and indirect receptor signaling in mice

cIAP1/2 antagonization by SMAC mimetic induces non-canonical NF-κB mediated TH 17 cell homotypic interactions and increases their resistance to shear stress.

The retinoic acid receptor drives neuroinflammation and fine tunes the homeostasis of interleukin-17-producing T cells

The cIAP ubiquitin ligases sustain type 3 gamma delta T and ILCs during aging to allow normal cutaneous and mucosal responses

The immune checkpoint receptor associated phosphatases SHP‐1 and SHP‐2 are not required for γδT17 cell development, activation, or skin inflammation

The cIAP ubiquitin ligases sustain type 3 γδ T and innate lymphoid cells during aging to allow normal cutaneous and mucosal responses

The neonatal microenvironment programs innate γδ T cells through the transcription factor STAT5