Programmed cell death and extrathymic reduction of Vβ8+CD4+ T cells in mice tolerant to Staphylococcus aureus enterotoxin B

Nature ◽  
1991 ◽  
Vol 349 (6306) ◽  
pp. 245-248 ◽  
Author(s):  
Yojiro Kawabe ◽  
Atsuo Ochi
Keyword(s):  
Staphylococcus Aureus ◽  
T Cells ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Cd4 T Cells ◽  
Enterotoxin B ◽  
Staphylococcus Aureus Enterotoxin B

scholarly journals Low programmed cell death-1 (PD-1) expression in peripheral CD4+T cells in Japanese patients with autoimmune type 1 diabetes

2015 ◽  
Vol 180 (3) ◽  
pp. 452-457 ◽  
Author(s):  
R. Fujisawa ◽  
F. Haseda ◽  
C. Tsutsumi ◽  
Y. Hiromine ◽  
S. Noso ◽  
...  
Keyword(s):  
T Cells ◽  
Cell Death ◽  
Type 1 Diabetes ◽  
Programmed Cell Death ◽  
Cd4 T Cells ◽  
Japanese Patients ◽  
Programmed Cell Death 1

scholarly journals Immune checkpoint dysfunction in large and medium vessel vasculitis

2017 ◽  
Vol 312 (5) ◽  
pp. H1052-H1059 ◽  
Author(s):  
Ryu Watanabe ◽  
Hui Zhang ◽  
Gerald Berry ◽  
Jörg J. Goronzy ◽  
Cornelia M. Weyand
Keyword(s):  
T Cells ◽  
Cell Death ◽  
T Cell ◽  
Programmed Cell Death ◽  
Immune Checkpoint ◽  
Intimal Hyperplasia ◽  
Cd4 T Cells ◽  
Vessel Wall ◽  
Checkpoint Inhibitors ◽  
Cell Death Protein

Giant cell arteritis (GCA) is a granulomatous vasculitis of the aorta and its medium-sized branch vessels. CD4 T cells, macrophages, and dendritic cells (DCs) build granulomatous infiltrates that injure the vessel wall and elicit a maladaptive response to injury. Pathological consequences include fragmentation of elastic membranes, destruction of the medial layer, microvascular neoangiogenesis, massive outgrowth of myofibroblasts, and lumen-occlusive intimal hyperplasia. Antigens have been suspected to drive the local activation of vasculitogenic CD4 T cells, but recent data have suggested a more generalized defect in the threshold setting of such T cells, rendering them hyperreactive. Under physiological conditions, immune checkpoints provide negative signals to curb T cell activation and prevent inflammation-associated tissue destruction. This protective mechanism is disrupted in GCA. Vessel wall DCs fail to express the immunoinhibitory ligand programmed cell death ligand-1, leaving lesional T cells unchecked. Consequently, programmed cell death protein-1-positive CD4 T cells can enter the immunoprivileged vessel wall, where they produce a broad spectrum of inflammatory cytokines (interferon-γ, IL-17, and IL-21) and have a direct role in driving intimal hyperplasia and intramural neoangiogenesis. The deficiency of the programmed cell death protein-1 immune checkpoint in GCA, promoting unopposed T cell immunity, contrasts with checkpoint hyperactivity in cancer patients in whom excessive programmed cell death ligand-1 expression paralyzes the function of antitumor T cells. Excessive checkpoint activity is the principle underlying cancer-immune evasion and is therapeutically targeted by immunotherapy with checkpoint inhibitors. Such checkpoint inhibitors, which unleash anticancer T cells and induce immune-related toxicity, may lead to drug-induced vasculitis.

Differential Induction of Programmed Cell Death in CD8+and CD4+T Cells by the B Subunit of Cholera Toxin

1996 ◽  
Vol 168 (2) ◽  
pp. 229-234 ◽  
Author(s):  
Boris Yankelevich ◽  
Viatcheslav A. Soldatenkov ◽  
Jennifer Hodgson ◽  
Alex J. Polotsky ◽  
Karen Creswell ◽  
...  
Keyword(s):  
T Cells ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Cholera Toxin ◽  
Cd4 T Cells ◽  
B Subunit ◽  
Differential Induction

scholarly journals Cell-Based Measures of Viral Persistence Are Associated With Immune Activation and Programmed Cell Death Protein 1 (PD-1)–Expressing CD4+ T cells

2012 ◽  
Vol 208 (1) ◽  
pp. 50-56 ◽  
Author(s):  
Hiroyu Hatano ◽  
Vivek Jain ◽  
Peter W. Hunt ◽  
Tzong-Hae Lee ◽  
Elizabeth Sinclair ◽  
...  
Keyword(s):  
T Cells ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Immune Activation ◽  
Cd4 T Cells ◽  
Viral Persistence ◽  
Cell Death Protein
Sign in / Sign up

Export Citation Format

Share Document