title: Regulatory T cells contribute to the recovery of acute lung injury by upregulating Tim-3.
abstract: Acute lung injury (ALI) is characterized by alveolar injury and uncontrolled inflammation. Mechanisms underlying pathogenesis of ALI are unknown. Regulatory T cells (Tregs), either natural or induced, suppress a variety of physiological and pathological immune responses. In the current study, we investigated whether Tregs were involved in the development of ALI. Proportion of CD4+CD25+FoxP3+ Tregs in the peripheral blood of 66 ALI patients and 30 healthy controls were examined by flow cytometry. Data showed that the percentage of Tregs in CD4+ T cells was significantly increased in patients than that in controls (10.8 versus 7.6%, P=0.003). Also, compared to those who died during the study, patients who survived presented significantly higher level of Tregs at the time of recruitment (P=0.041). Since Tim-3 is a negative regulatory molecule and can modulate the function of Tregs, we evaluated Tim-3 level on Tregs and identified upregulation of the molecule in patients than that in controls. Moreover, compared to those who died during the study, patients who survived showed 1.7-fold higher level of Tim-3 on Tregs at the time of recruitment (P<0.001). These results suggest that Tregs could affect the prognosis of ALI probably due to the upregulation of Tim-3.
authors.affiliation: Department of Internal Medicine, Emergency Center East Hospital, Tongji University School of Medicine, 150 Jimo Road, Shanghai, 200120, China.
authors.forename: Haihan
authors.initials: H
authors.lastname: Song
authors.forename: Yujia
authors.initials: Y
authors.lastname: Zhou
authors.forename: Guanggang
authors.initials: G
authors.lastname: Li
authors.forename: Jianwen
authors.initials: J
authors.lastname: Bai
mesh_terms: D055371:Acute Lung Injury / Q000276:immunology* / Q000401:mortality* / Q000473:pathology; D000368:Aged; D015704:CD4 Antigens / Q000378:metabolism; D005260:Female; D051858:Forkhead Transcription Factors / Q000378:metabolism; D000072597:Hepatitis A Virus Cellular Receptor 2; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000473:pathology; D053645:Interleukin-2 Receptor alpha Subunit / Q000378:metabolism; D018655:Lymphocyte Count; D008297:Male; D008565:Membrane Proteins / Q000096:biosynthesis*; D008875:Middle Aged; D011379:Prognosis; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*; D015854:Up-Regulation
chemical_list: D015704:CD4 Antigens; D051858:Forkhead Transcription Factors; C498833:Foxp3 protein, mouse; C448908:HAVCR2 protein, human; D000072597:Hepatitis A Virus Cellular Receptor 2; D053645:Interleukin-2 Receptor alpha Subunit; D008565:Membrane Proteins