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CD8A — TNF

Text-mined interactions from Literome

El-Sheikh et al., J Autoimmun 1999 (Diabetes Mellitus, Type 1) : Depletion of either CD4 ( + ) or CD8 ( + ) T cells may prevent beta-cell destruction by decreasing IFN-gamma and IL-10 production in islets and increasing IL-4 and TNF-alpha production systemically
Liu et al., Am J Respir Cell Mol Biol 1999 : Perforin independent CD8 ( + ) T-cell mediated cytotoxicity of alveolar epithelial cells is preferentially mediated by tumor necrosis factor-alpha : relative insensitivity to Fas ligand
Kafrouni et al., J Immunol 2001 : Delayed clearance of AdCMV-lacZ from the livers of FasL-defective B6.gld mice, but not perforin-deficient B6.pfp ( -/- ) mice, was noted despite no significant differences in initial hepatic CD8 ( + ) T cell IFN-gamma or TNF responses or in activation of intrahepatic cytotoxic lymphocytes cells capable of killing AdCMV-lacZ infected fibroblast targets
Suda et al., J Immunol 1992 : Of 15 cytokines tested, only transforming growth factor ( TGF-beta ) and TNF-alpha induced CD8 ( Lyt-2 ), while no cytokine was able to induce CD4 on CD25+CD3-CD4-CD8- thymocytes ... In contrast, neither TGF-beta nor TNF-alpha induced CD8 expression on splenic CD4+CD8- T cells
Soldan et al., J Immunol 2003 (Multiple Sclerosis, Chronic Progressive...) : The increase in IL-5 was primarily due to an increase in CD4 ( + ) and CD8 ( + ) T cells, the increase in IL-10 was primarily due to an increase in CD64 ( + ) monocytes/macrophages with some effect in T cells, while the decrease in TNF-alpha was primarily due to a decrease in CD8 ( + ) T cells
Shinbori et al., Eur J Immunol 2004 (Lung Diseases, Interstitial) : Furthermore, we found that the interaction of SEB stimulated CD8 ( + ) CTL with lung epithelial cells induced an increase in TNF-alpha secretion
Suresh et al., J Virol 2005 (Acute Disease...) : Role of tumor necrosis factor receptors in regulating CD8 T-cell responses during acute lymphocytic choriomeningitis virus infection ... To address these issues, we have investigated the role of tumor necrosis factor receptors (TNFRs) I ( p55R ) and II ( p75R ) in regulating CD8 T-cell responses to lymphocytic choriomeningitis virus ( LCMV ) with wild-type, p55R-deficient ( p55 ( -/- ) ), p75R-deficient ( p75 ( -/- ) ), and p55R- and p75R-deficient ( DKO ) mice
Poggi et al., Eur J Immunol 2005 : The engagement of CD8 or activating KIR also triggered the production of TNF-alpha
Lang et al., J Clin Invest 2006 (Liver Diseases) : While TLR3 activation did not directly alter liver-specific CD8+ T cell function, it induced IFN-alpha and TNF-alpha release
Bertolino et al., Hepatology 2007 : While TLR3 activation did not directly alter liver-specific CD8+ T cell function, it induced IFN-alpha and TNF-alpha release
Shi et al., Biochem Biophys Res Commun 2007 : Alpha tumor necrosis factor contributes to CD8 ( + ) T cell survival in the transition phase ... In contrast, TNF-alpha deficiency in both recipients and donor CD8 ( + ) effector T cells significantly reduced CD8 ( + ) T cell survival
Singh et al., J Leukoc Biol 2007 (Lymphocytic Choriomeningitis) : Collectively, these data are strongly suggestive of a role for TNF in down regulating CD8 T cell responses and the establishment of CD8 T cell memory during an acute viral infection
Zhang et al., J Clin Invest 2007 (Influenza, Human...) : Elevated levels of IL-10 early in the response was key to the loss of CD4 ( + ) T cells, whereas CD8 ( + ) T cell deletion was dependent on a prolonged TNF-alpha response, IL-10, and upregulation of Fas
Wong et al., J Immunol 2009 : IL-12p70 production was produced predominantly by CD8alpha ( + ) DCs and plasmacytoid DCs, and mediated by CD8 T cell derived cytokines IFN-gamma, GM-CSF, TNF-alpha , and surface CD40L
Andrade et al., J Acquir Immune Defic Syndr 2010 (Acquired Immunodeficiency Syndrome) : CD8 ( + ) T lymphocytes depletion reduced IL-1beta and TNF-alpha release in the older groups, however, it did not significantly alter their IFN-gamma production
Freeman et al., J Immunol 2010 (Pulmonary Disease, Chronic Obstructive) : In vitro stimulation of lung CD8 ( + ) T cells with IL-18 plus IL-12 markedly increased production of IFN-gamma and TNF-alpha , whereas IL-15 stimulation induced increased intracellular perforin expression
Ablamunits et al., Eur J Immunol 2010 (Diabetes Mellitus, Type 1) : The induction of CD8 ( + ) Treg by anti-CD3 mAb requires TNF and signaling through the NF-?B cascade
Frick et al., Eur J Pharmacol 2011 (Lymphoma) : These changes were accompanied by increased IFN-? and TNF-a levels as well as augmented circulating CD8 ( + ) T lymphocytes in tumor bearing mice treated with the antidepressant
Robinet et al., J Immunol 1990 : TNF did not affect the expression of LFA1, CD2, CD4, and CD8 , molecules that are associated with CTL-target interactions, on responder cells
Ding et al., J Immunol 2011 (Coronavirus Infections) : TNF receptor 1 mediates dendritic cell maturation and CD8 T cell response through two distinct mechanisms
Tittarelli et al., Cancer Immunol Immunother 2012 (Melanoma...) : Antibody blocking of monocyte TLR4 inhibited surface expression, determined by flow cytometry, of the major histocompatibility complex class I, CCR7, CD80, CD83 and CD86 on TAPCells, reduced interleukin (IL)-6 and tumor necrosis factor -a gene expression evaluated by qRT-PCR, and also inhibited the TAPCells mediated interferon-? ( IFN-? ) secretion of melanoma-specific CD8 ( + ) T cells determined by ELISpot ( p < 0.01 )
Soloviova et al., J Immunol 2013 (Graft vs Host Disease) : A useful model for in vivo CD8 CTL in the absence of exogenous pathogens is the alloantigen-driven parent-into F1 model of acute graft-versus-host disease ( GVHD ) characterized by a strong TNF dependent donor antihost CD8 CTL T cell response
Martín et al., Hepatology 1994 (Chronic Disease...) : To assess changes in immune function during therapy of chronic hepatitis B patients, spontaneous and mitogen induced production of tumor necrosis factor-alpha, interleukin-1 beta, interleukin-6, interferon-alpha and interferon-gamma were measured-along with serum levels of soluble CD4, soluble CD8 , soluble interleukin-2 receptor and beta 2-microglobulin-before, during and after a 6-wk course of granulocyte-macrophage colony stimulating factor in nine patients with chronic hepatitis B. Treatment statistically enhanced spontaneous production of tumor necrosis factor-alpha ( p < 0.05 ) and interleukin-1 beta ( p < 0.02 )