title: Interleukin-13 interferes with activation-induced t-cell apoptosis by repressing p53 expression.
abstract: The etiology and the underlying mechanism of CD4(+) T-cell polarization are unclear. This study sought to investigate the mechanism by which interleukin (IL)-13 prevents the activation-induced apoptosis of CD4(+) T cells. Here we report that CD4(+) T cells expressed IL-13 receptor α2 in the intestine of sensitized mice. IL-13 suppressed both the activation-induced apoptosis of CD4(+) T cells and the expression of p53 and FasL. Exposure to recombinant IL-13 inhibited activation-induced cell death (AICD) along with the expression of p53, caspase 3, and tumor necrosis factor-α in CD4(+) T cells. Administration of an anti-IL-13 antibody enhanced the effect of specific immunotherapy on allergic inflammation in the mouse intestine, enforced the expression of p53 in intestinal CD4(+) T cells, and enhanced the frequency of CD4(+) T-cell apoptosis upon challenge with specific antigens. In summary, blocking IL-13 enhances the therapeutic effect of antigen-specific immunotherapy by regulating apoptosis and thereby enforcing AICD in CD4(+) T cells.
authors.affiliation: Department of Gastroenterology, the Zhengzhou People's Hospital, Zhengzhou, China.|Department of Gastroenterology, the Fifth Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
authors.forename: Li
authors.initials: L
authors.lastname: Yang
authors.affiliation: Shenzhen Key Laboratory of Allergy and Immunology, Shenzhen University School of Medicine and State Key Laboratory of Respiratory Disease for Allergy at Shenzhen University, Shenzhen, China.
authors.forename: Ling-Zhi
authors.initials: LZ
authors.lastname: Xu
authors.affiliation: Shenzhen Key Laboratory of Allergy and Immunology, Shenzhen University School of Medicine and State Key Laboratory of Respiratory Disease for Allergy at Shenzhen University, Shenzhen, China.|ENT Institute of Shenzhen University, Longgang Central Hospital, Shenzhen, China.|ENT Institute of Shenzhen University, Longgang Central Hospital, Shenzhen, China.
authors.forename: Zhi-Qiang
authors.initials: ZQ
authors.lastname: Liu
authors.affiliation: Shenzhen Key Laboratory of Allergy and Immunology, Shenzhen University School of Medicine and State Key Laboratory of Respiratory Disease for Allergy at Shenzhen University, Shenzhen, China.|ENT Institute of Shenzhen University, Longgang Central Hospital, Shenzhen, China.|ENT Institute of Shenzhen University, Longgang Central Hospital, Shenzhen, China.
authors.forename: Gui
authors.initials: G
authors.lastname: Yang
authors.affiliation: Shenzhen Key Laboratory of Allergy and Immunology, Shenzhen University School of Medicine and State Key Laboratory of Respiratory Disease for Allergy at Shenzhen University, Shenzhen, China.|ENT Institute of Shenzhen University, Longgang Central Hospital, Shenzhen, China.|ENT Institute of Shenzhen University, Longgang Central Hospital, Shenzhen, China.
authors.forename: Xiao-Rui
authors.initials: XR
authors.lastname: Geng
authors.affiliation: Shenzhen Key Laboratory of Allergy and Immunology, Shenzhen University School of Medicine and State Key Laboratory of Respiratory Disease for Allergy at Shenzhen University, Shenzhen, China.
authors.forename: Li-Hua
authors.initials: LH
authors.lastname: Mo
authors.affiliation: Shenzhen Key Laboratory of Allergy and Immunology, Shenzhen University School of Medicine and State Key Laboratory of Respiratory Disease for Allergy at Shenzhen University, Shenzhen, China.
authors.forename: Zhi-Gang
authors.initials: ZG
authors.lastname: Liu
authors.affiliation: Department of Gastroenterology, the Fifth Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
authors.forename: Peng-Yuan
authors.initials: PY
authors.lastname: Zheng
authors.affiliation: Shenzhen Key Laboratory of Allergy and Immunology, Shenzhen University School of Medicine and State Key Laboratory of Respiratory Disease for Allergy at Shenzhen University, Shenzhen, China.
authors.forename: Ping-Chang
authors.initials: PC
authors.lastname: Yang
mesh_terms: D000818:Animals; D000941:Antigens / Q000378:metabolism; D017209:Apoptosis / Q000276:immunology*; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D016923:Cell Death; D016764:Cell Polarity; D000939:Epitopes; D053222:Fas Ligand Protein / Q000378:metabolism; D006967:Hypersensitivity / Q000276:immunology; D007167:Immunotherapy; D018793:Interleukin-13 / Q000378:metabolism*; D007422:Intestines / Q000276:immunology / Q000473:pathology; D008213:Lymphocyte Activation / Q000276:immunology*; D008297:Male; D008807:Mice, Inbred BALB C; D053660:Receptors, Interleukin-13 / Q000378:metabolism; D013601:T-Lymphocytes / Q000166:cytology* / Q000276:immunology*; D014158:Transcription, Genetic; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism*; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D000941:Antigens; D000939:Epitopes; D053222:Fas Ligand Protein; D018793:Interleukin-13; D053660:Receptors, Interleukin-13; D014409:Tumor Necrosis Factor-alpha; D016159:Tumor Suppressor Protein p53; D051028:bcl-2-Associated X Protein