ArticleImmunology1999
Increased inducible apoptosis in CD4+ T lymphocytes during polymicrobial sepsis is mediated by Fas ligand and not endotoxin.
Article in Immunology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 72 citations in OpenAlex.
- Microarray Analysis Reveals Sepsis Is a Syndrome with Hyperactivity of TH17 Immunity, with Over-Presentation of the Treg Cell Cytokine TGF-β.Current issues in molecular biology · 2025Article
- Effects of simvastatin on the function of splenic CD4Immunologic research · 2018Article
- The protective role of human ghrelin in sepsis: Restoration of CD4 T cell proliferation.PloS one · 2018Article
- A new mass spectrometry-based method for the quantification of histones in plasma from septic shock patients.Scientific reports · 2017Article
- Role of Mitochondrial DNA in Septic AKI via Toll-Like Receptor 9.Journal of the American Society of Nephrology : JASN · 2016Article
- Alterations of dendritic cells in sepsis: featured role in immunoparalysis.BioMed research international · 2015Review
- Revisiting caspases in sepsis.Cell death & disease · 2014Review
- Overexpression of Fas and FasL is associated with infectious complications and severity of experimental severe acute pancreatitis by promoting apoptosis of lymphocytes.Inflammation · 2014Article
- The role of Fas expression on the occurrence of immunosuppression in severe acute pancreatitis.Digestive diseases and sciences · 2013Article
- Burn-injury affects gut-associated lymphoid tissues derived CD4+ T cells.Results in immunology · 2013Article
- Prevention of lymphocyte apoptosis in septic mice with cancer increases mortality.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Epigenetic regulation of immune cell functions during post-septic immunosuppression.Epigenetics · 2011Review
- Article
- Impaired CD4+ T-cell proliferation and effector function correlates with repressive histone methylation events in a mouse model of severe sepsis.European journal of immunology · 2010Article
- Immature dendritic cell-derived exosomes rescue septic animals via milk fat globule epidermal growth factor-factor VIII [corrected].Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- Enhanced T-cell apoptosis in human septic shock is associated with alteration of the costimulatory pathway.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2009Article
- VX-166: a novel potent small molecule caspase inhibitor as a potential therapy for sepsis.Critical care (London, England) · 2009Article
- Second hit post burn increased proximal gut mucosa epithelial cells damage.Shock (Augusta, Ga.) · 2008Article
- Regulatory roles of CD1d-restricted NKT cells in the induction of toxic shock-like syndrome in an animal model of fatal ehrlichiosis.Infection and immunity · 2008Article
- Thermal injury-plus-sepsis contributes to a substantial deletion of intestinal mesenteric lymph node CD4 T cell via apoptosis.International journal of biological sciences · 2007Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Recent studies suggest that increased lymphocyte apoptosis (Ao) detected in peripheral blood T cells from burn patients appears to contribute to decreased lymphocyte immunoresponsiveness. However, while it is known that sepsis induces a marked depression in the splenocyte immune response (i.e. decreased interleukin-2, interferon-gamma production and proliferation) in response to the T-cell mitogen concanavalin A (Con A), it is unknown whether this depression is associated with an increase in inducible Ao and if so, which mediators control this process. To assess this, splenocytes were harvested from mice at 24 hr (a period associated with decreased Con A response) after the onset of polymicrobial sepsis [caecal ligation and puncture (CLP)] or sham-CLP (Sham) and then stimulated with 2.5 microg Con A/ml (24 hr). Septic mouse splenocytes stimulated with Con A, while not showing a change in their phenotypic make-up, did exhibit a marked increase in the percentage of splenocyte that were Ao+ which was associated with altered cytokine release. This appears to be due to an increase in the percentage of Ao+ cells in the CD4+ CD8- population and was associated with enhanced Fas antigen expression as well as an increase in mRNA for the Fas-FasL gene family. To determine if the changes in Ao are due to either endotoxin (a product of Gram-negative bacteria seen in CLP mice) or the expression of Fas ligand (FasL; a mediator of activation-induced lymphocyte Ao), a second set of studies examining Con A-inducible Ao was performed with splenocytes harvested from septic endotoxin-tolerant C3H/HeJ and the FasL-deficient C3H/HeJ-Fasl gld mice. The results show that increased splenocyte Ao detected following CLP is due to a FasL-mediated process and not to endotoxin. Thus the inadvertent up-regulation of FasL-mediated splenocyte Ao may contribute to the depression of splenocyte immune responses seen during polymicrobial sepsis.
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