• Aharon Kessel, Ellen Bamberger, Muhamad Masalha, and Elias Toubi.
• Division of Allergy and Clinical Immunology, Bnai-Zion Medical Center, The Bruce Rappaport Faculty of Medicine, Technion, Haifa, Israel.
• J. Autoimmun. 2009 May 1; 32 (3-4): 211-5.

AbstractIt is well-known that septic shock undermines immune homeostasis by inducing an initial intense systemic inflammatory response that is rapidly followed by a negative feedback of anti-inflammatory process. This secondary immunoparalysis state is characterized by decreased phagocytic cells, T cells, natural killer cells and B cells function and proinflammatory cytokine release. This persistence of immunoparalysis increased the risk for fatal outcome. In recent studies it was found that following the onset of septic shock, a relative increase in T regulatory cells number and suppressive function appears and makes them an important participant in the inhibition of immune responsiveness during sepsis. Consequently, a question emerging from these findings concerns the degree to which the manipulation of T regulatory cells might improve the outcome of patients with sepsis. Preliminary studies in animal models suggest that more work is needed to understand the conditions under which such a therapy may be effective.

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