ArticleThe American journal of pathology2009
Suppression of activation and costimulatory signaling in splenic CD4+ T cells after trauma-hemorrhage reduces T-cell function: a mechanism of post-traumatic immune suppression.
Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- Targeting Inflammation After Hemorrhagic Shock as a Molecular and Experimental Journey to Improve Outcomes: A Review.Cureus · 2025Review
- Mitochondrial dysfunction in rat splenocytes following hemorrhagic shock.Biochimica et biophysica acta. Molecular basis of disease · 2017Article
- Anti-HMGB1 monoclonal antibody ameliorates immunosuppression after peripheral tissue trauma: attenuated T-lymphocyte response and increased splenic CD11b (+) Gr-1 (+) myeloid-derived suppressor cells require HMGB1.Mediators of inflammation · 2015Article
- Dynamic changes of circulating T-helper cell subsets following severe thoracic trauma.International journal of clinical and experimental medicine · 2015Article
- OX62+OX6+OX35+ rat dendritic cells are unable to prime CD4+ T cells for an effective immune response following acute burn injury.Results in immunology · 2013Article
- Immune system phenotyping of radiation and radiation combined injury in outbred mice.Radiation research · 2013Article
- Additive effects of exogenous IL-12 supplementation and antibiotic treatment in infection prophylaxis.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2012Article
- Effects of trauma-hemorrhage and IL-6 deficiency on splenic immune function in a murine trauma model.Mediators of inflammation · 2012Article
- Macrophage-produced IL-12p70 mediates hemorrhage-induced damage in a complement-dependent manner.Shock (Augusta, Ga.) · 2011Article
- Experimental trauma models: an update.Journal of biomedicine & biotechnology · 2011Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Reduced immune function is frequently a consequence of serious injury such as trauma-hemorrhage (T-H). Injury may lead to reduced T-cell activation, resulting in decreased engagement of costimulatory molecules after antigen recognition and in subsequent immunological compromise and anergy. We hypothesized that inhibition of CD28 expression is one possible mechanism by which immune functions are suppressed after T-H. Male C3H/HeN mice (with or without ovalbumin immunization) were subjected to sham operation or T-H and sacrificed after 24 hours. Splenic T cells were then stimulated with concanavalin A or ovalbumin in vivo or in vitro, and CD28, cytotoxic T-lymphocyte antigen 4 (CTLA-4), CD69, and phospho-Akt expression was determined. T-cell proliferation/cytokine production was measured in vitro. Stimulation-induced CD69, CD28, and phospho-Akt up-regulation were significantly impaired after T-H compared with sham-operated animals; however, CTLA-4 expression was significantly higher in the T-H group. Over a 3-day span, stimulated T cells from sham-operated animals showed significantly higher proliferation compared with the T-H group. IL-2 and IFN-gamma were elevated in sham-operated animals, whereas IL-4 and IL-5 rose in the T-H group, revealing a shift from T(H)1 to T(H)2 type cytokine production after T-H. Dysregulation of the T-cell costimulatory pathway is therefore likely to be a significant contributor to post-traumatic immune suppression.
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