tailieunhanh - Báo cáo hóa học: "IL-2 as a therapeutic target for the restoration of Foxp3+ regulatory T cell function in organ-specific autoimmunity: implications in pathophysiology and translation to human disease"

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành hóa học dành cho các bạn yêu hóa học tham khảo đề tài: IL-2 as a therapeutic target for the restoration of Foxp3+ regulatory T cell function in organ-specific autoimmunity: implications in pathophysiology and translation to human disease | H JOURNAL OF TRANSLATIONAL MEDICINE IL-2 as a therapeutic target for the restoration of Foxp3 regulatory T cell function in organ-specific autoimmunity implications in pathophysiology and translation to human disease d Hennezel et al. d Hennezel et al. Journal of Translational Medicine 2010 8 113 http content 8 1 113 8 November 2010 BioMed Central d Hennezel et al. Journal of Translational Medicine 2010 8 113 http content 8 1 113 REVIEW JOURNAL OF TRANSLATIONAL MEDICINE Open Access IL-2 as a therapeutic target for the restoration of Foxp3 regulatory T cell function in organ-specific autoimmunity implications in pathophysiology and translation to human disease Eva d HennezeP Mara KorneteH Ciriaco A Piccirillo2 Abstract Peripheral immune tolerance requires a finely controlled balance between tolerance to self-antigens and protective immunity against enteric and invading pathogens. Self-reactive T cells sometimes escape thymic clonal deletion and can subsequently provoke autoimmune diseases such as type 1 diabetes T1D unless they are controlled by a network of tolerance mechanisms in the periphery including CD4 regulatory T cells Treg cells. CD4 Treg cells are characterized by the constitutive expression of the IL-2Ra chain CD25 and preferentially express the forkhead winged helix transcriptional regulator Foxp3. These cells have been shown to possess immunosuppressive properties towards various immune cell subsets and their defects are thought to contribute to many autoimmune disorders. Strong evidence shows that IL-2 is one of the important stimulatory signals for the development function and fitness of Treg cells. The non-obese diabetic NOD mouse model a prototypic model of spontaneous autoimmunity mimics many features of human T1 D. Using this model the contribution of the IL-2-IL-2R pathway to the development of T1 D and other autoimmune disorders has been extensively studied. In the past years strong