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CASP1 — CD8A

Text-mined interactions from Literome

Thoma-Uszynski et al., J Immunol 2000 : However, both DN and CD8 ( + ) CTL induced nuclear apoptosis required caspase activation
Ruiz et al., Clin Immunol 2001 : These findings demonstrate that intracellular caspase-1- and -3-like enzyme activity increases in both CD4 ( + ) and CD8 ( + ) alloreactive T cells as the primary response to allostimulatory cells progresses
Prins et al., Cancer Immunol Immunother 2001 (Brain Neoplasms...) : In vitro, the downregulation of CD8beta could be inhibited by the caspase inhibitor, z-VAD
Quan et al., Med Oncol 2009 : To ascertain the mechanism of endothelial apoptosis, we determined that allogeneic CD8 ( + ) T cell, SFLLRN enhanced cleavage of caspase-3 and led to p38MAPK activation as assessed by Western blot
Ichinohe et al., J Exp Med 2009 (Orthomyxoviridae Infections) : Although NLRP3 was required for inflammasome activation in certain cell types, CD4 and CD8 T cell responses, as well as mucosal IgA secretion and systemic IgG responses, required ASC and caspase-1 but not NLRP3
Murakami et al., Eur J Immunol 2010 : Surprisingly, our studies demonstrate that caspase 3 was not required for the induction of CD8 ( + ) T-cell anergy in vivo, contrary to published reports using CD4 ( + ) T cells
Lacerda-Queiroz et al., Am J Pathol 2012 (Malaria, Cerebral) : In PAFR ( -/- ) mice, lethality was markedly delayed and brain inflammation was significantly reduced, as demonstrated by histology, accumulation, and activation of CD8 ( + ) T cells, changes in vascular permeability and activation of caspase-3 on endothelial cells and leukocytes