Sepsis is a severe complication which is usually caused by microbial infection,severe burns or trauma and major operations.Patients with sepsis were usually complicated with systemic inflammatory response and multi-organ dysfunction syndrome,which is the leading cause of death in the intensive care units.However,the main immunoregulatory mechanisms underlying severe sepsis remain unclear,and effective methods for monitoring immune status and immunomodulatory strategies need to be investigated.In recent years,the understanding of the mechanism of sepsis has been developed.Clinicians have learned that immune dysfunction took part in the pathophysiological process of sepsis.Therefore,rational monitoring of immune status in patients with severe sepsis after burns or major operation,seeking effective ways for diagnosis,treatment and intervention are of great significance in decreasing the mortality and improving the life quality.

With rapid progress and dangerous prognosis, traumatic brain injury (TBI) brings great difficulties in the clinical treatment, which becomes a prominent problem for the modern emergency and critical care medicine. In addition to the necessary surgical intervention under special circumstances, there are new understandings about the clinical management measures, noninvasive and invasive monitoring mode of TBI in recent years. This review provides a summary of the monitoring and treatment on the TBI, with our deep understanding of regulatory mechanism underlying TBI, precise modulation might be of clinical significance in preventing secondary damage of tissues and organs, which would be associated with decreases in the disability and mortality of critically ill patients.

Objective To observe the expression of tumor necrosis factor-α induced protein 8 like-2 (TIPE2) in CD4 + CD25 + regulatory T cells ( CD4 + CD25 + Tregs) and analyze its potential effect on immunosuppressive activity of CD4 + CD25 + Tregs. Methods CD4 + CD25 + Tregs were purified from spleen of the BALB/c mice by using magnetic cell sorting system.The expressions of TIPE2 mRNA and protein in CD4 + CD25 + Tregs were detected by using RT-PCR and Western blot.CD4 + CD25 +Tregs were further infected with the recombinant lentiviruses that carried small interference RNA(siRNA)to knock down the TIPE2 expression.Based on the expressions of cell surface molecules including cytotoxic T-lymphocyte-associated antigen (CTLA)-4 and forkhead/winged helix transcription factor p3 (Foxp3) detected by flow cytometry and the levels of cytokines including interleukin (IL)-10 and transforming growth factor (TGF)-3 examined by ELISA in CD4 + CD25 + Tregs,the functional role of TIPE2 in controlling suppressive activity of CD4 + CD25 + Tregs was analyzed.In the meantime,the proliferation activities of T effector cells were assayed by MTT test. Results A 147 bp TTPE2 gene band and a clear TIPE2 band with a molecular mass of approximately 21 000 in CD4 + CD25 + Tregs were detected by using Westem blot.Cell surface molecule as well as cytokine expressions were significantly down-regulated when the CD4 + CD25 + Treg stimulated and activated by anti-CD3/CD28 was cultured for 24 hours after the siRNA silenced CD4 + CD25 + Treg cells ( P ＜ 0.01 ).Meanwhile,the suppression role of CD4 +CD25 + Tregs on the proliferation activity of T effector cells was weakened obviously ( P ＜ 0.05 ). Conclusions As an important immunoregulatory molecule,TIPE2 not only expresses in the CD4 + CD25 +Tregs,but also affects the immunosuppressive function of CD4 + CD25 + Tregs.

Sepsis is caused by various pathogens and toxic factors, which can lead to multiple organ dysfunction. The underlying mechanism of sepsis appears to be complex, involving epigenetic reprogramming, metabolic failure, immune dysfunction, neuroendocrine system disorders, coagulation abnormalities, tissue or organ failure, and many other scientific issues. With our deep understanding of the host reaction and development of sepsis, it is of great significance to explore predicative markers and therapeutic targets according to the atypical characteristics of sepsis, thereby contributing to the reduction of morbidity and mortality of sepsis.