Dehydroepiandrosteron normalisiert die in einem standardisierten Sepsismodell der Maus unterdrückte Typ-IV-Immunreaktion

[1]  M. Grotz,et al.  Levels of antibodies to endotoxin and cytokine release in patients with severe trauma: does posttraumatic dysergy contribute to organ failure? , 1999, The Journal of trauma.

[2]  F. Svec,et al.  The Actions of Exogenous Dehydroepiandrosterone in Experimental Animals and Humans , 1998, Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine.

[3]  F. Dhabhar,et al.  Acute Stress Enhances while Chronic Stress Suppresses Cell-Mediated Immunityin Vivo:A Potential Role for Leukocyte Trafficking , 1997, Brain, Behavior, and Immunity.

[4]  T. Fabian,et al.  DEHYDROEPIANDROSTERONE, AN ENDOGENOUS IMMUNE MODULATOR, AFTER TRAUMATIC SHOCK , 1997, Shock.

[5]  R. Daynes,et al.  Dehydroepiandrosterone functions as more than an antiglucocorticoid in preserving immunocompetence after thermal injury. , 1995, Endocrinology.

[6]  L. Napolitano,et al.  Polymicrobial sepsis following trauma inhibits interleukin-10 secretion and lymphocyte proliferation. , 1994, The Journal of trauma.

[7]  J. Mannick,et al.  Cytokines, sepsis and immunomodulation , 1993, The British journal of surgery.

[8]  D. Ben-Nathan,et al.  Dehydroepiandrosterone protects mice from endotoxin toxicity and reduces tumor necrosis factor production , 1992, Antimicrobial Agents and Chemotherapy.

[9]  G. Regel,et al.  [Multiple organ failure. Reflection of generalized cell damage of all organs following severe trauma]. , 1991, Der Unfallchirurg.