{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,7]],"date-time":"2026-05-07T06:26:17Z","timestamp":1778135177457,"version":"3.51.4"},"reference-count":48,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Endocrinology and Metabolism"],"published-print":{"date-parts":[[2010,8]]},"abstract":"<jats:p>Glucocorticoids (GC) are steroid hormones that modulate T cell functions and restrain their hyperresponsiveness following stimulation. Naive T lymphocytes are sensitive to GC but become more resistant when they are activated. A balance between activation and inhibition signals is important for a targeted and effective T cell response. Thermal injury is characterized by an immune dysfunction and hyperactive T cells visible at day 10 postburn. In this study, our objective was to evaluate T cell sensitivity to GC following thermal injury and to identify mechanisms that could modulate their sensitivity. One mechanism that we hypothesized was increased p38 mitogen-activated protein kinase (MAPK) activity that could lead to GC resistance. Male C57BL\/6 mice underwent a full-thickness 20% total body surface area. At 10 days postinjury, splenic T cells were isolated. Glucocorticoid receptor (GR) expression was higher in T cells from burn-injured mice. Interestingly, these cells were also less sensitive to GC-induced apoptosis prior to and poststimulation. Furthermore, anti-CD3-activated T cells from burn-injured mice showed increased proliferation and CD25 expression, which resisted corticosterone's (CORT) suppressive effect. Anti-CD3-activated CD4<jats:sup>+<\/jats:sup>CD44<jats:sup>+<\/jats:sup>memory cells from burn-injured mice expressed the highest level of CD25 and were resistant to CORT. Increased phosphorylation of p38 MAPK was also noted in activated T cells from burn-injured mice. Pharmacological inhibition of p38 MAPK decreased cell proliferation and normalized interferon-\u03b3 (IFN\u03b3) production. In conclusion, we demonstrate that a unique event like burn injury induces a loss of sensitivity to GC in splenic T cells and have identified p38 MAPK as a key modulator for this resistance.<\/jats:p>","DOI":"10.1152\/ajpendo.00084.2010","type":"journal-article","created":{"date-parts":[[2010,6,2]],"date-time":"2010-06-02T00:58:36Z","timestamp":1275440316000},"page":"E299-E307","source":"Crossref","is-referenced-by-count":9,"title":["T cells from burn-injured mice demonstrate a loss of sensitivity to glucocorticoids"],"prefix":"10.1152","volume":"299","author":[{"given":"Michele","family":"D'Elia","sequence":"first","affiliation":[{"name":"Institut National de la Recherche Scientifique, Institut Armand-Frappier, Laval, Quebec, Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Julie","family":"Patenaude","sequence":"additional","affiliation":[{"name":"Institut National de la Recherche Scientifique, Institut Armand-Frappier, Laval, Quebec, 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