IL-2 controls trafficking receptor gene expression and Th2 response for skin and lung inflammation
Both Il2−/− mice and Scurfy (Sf) mutant mice that are deficient in FoxP3, develop multi-organ inflammation but only the latter display severe skin and lung inflammation. In contrast, Sf.Il2−/− double mutant mice do not display skin inflammation and markedly reduced lung inflammation. In this review,...
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Published in | Clinical immunology (Orlando, Fla.) Vol. 145; no. 1; pp. 82 - 88 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
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Elsevier Inc
01.10.2012
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Abstract | Both Il2−/− mice and Scurfy (Sf) mutant mice that are deficient in FoxP3, develop multi-organ inflammation but only the latter display severe skin and lung inflammation. In contrast, Sf.Il2−/− double mutant mice do not display skin inflammation and markedly reduced lung inflammation. In this review, we summarize our recent findings based on microarray, q-PCR and functional studies of 10 Sf double mutant mice. These studies revealed novel pro-inflammatory functions of IL-2 in regulating inflammation in an organ-specific manner. IL-2 exerts its “organ-specific” pro-inflammatory function by regulating the migration and retention of CD4+ T-cells (both Th1 and Th2) specifically to the skin and lung. In addition, IL-2 is also required for regulating the Th2 cytokine response during T-cell activation. Further studies on these IL-2‐regulated genes will help in identifying novel targets for intervention in inflammatory diseases of skin and lung.
► IL‐2 is an inflammatory cytokine for skin and lung as well as T‐cell growth. ► Th1 cytokine and related TRGs are insufficient to induce skin and lung inflammation. ► IL‐2 is required for the expression of many of the Th2 related traffic genes. ► IL-2 controls the expression of the adhesion molecule ITGAE, CD103. |
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AbstractList | Both Il2-/-mice and Scurfy (Sf) mutant mice that are deficient in FoxP3, develop multi-organ inflammation but only the latter display severe skin and lung inflammation. In contrast, Sf.Il2-/- double mutant mice do not display skin inflammation and markedly reduced lung inflammation. In this review, we summarize our recent findings based on microarray, q-PCR and functional studies of 10 Sf double mutant mice. These studies revealed novel pro-inflammatory functions of IL-2 in regulating inflammation in an organ-specific manner. IL-2 exerts its "organ-specific" pro-inflammatory function by regulating the migration and retention of CD4+ T-cells (both Th1 and Th2) specifically to the skin and lung. In addition, IL-2 is also required for regulating the Th2 cytokine response during T-cell activation. Further studies on these IL-2-regulated genes will help in identifying novel targets for intervention in inflammatory diseases of skin and lung. Both Il2 −/− mice and Scurfy (Sf) mutant mice that are deficient in FoxP3, develop multi-organ inflammation but only the latter display severe skin and lung inflammation. In contrast, Sf.Il2 −/− double mutant mice do not display skin inflammation and markedly reduced lung inflammation. In this review, we summarize our recent findings based on microarray, q -PCR and functional studies of 10 Sf double mutant mice. These studies revealed novel pro-inflammatory functions of IL-2 in regulating inflammation in an organ-specific manner. IL-2 exerts its “organ-specific” pro-inflammatory function by regulating the migration and retention of CD4 + T-cells (both Th1 and Th2) specifically to the skin and lung. In addition, IL-2 is also required for regulating the Th2 cytokine response during T-cell activation. Further studies on these IL-2 –regulated genes will help in identifying novel targets for intervention in inflammatory diseases of skin and lung. Abstract Both Il2 −/− mice and Scurfy (Sf) mutant mice that are deficient in FoxP3, develop multi-organ inflammation but only the latter display severe skin and lung inflammation. In contrast, Sf.Il2 −/− double mutant mice do not display skin inflammation and markedly reduced lung inflammation. In this review, we summarize our recent findings based on microarray, q -PCR and functional studies of 10 Sf double mutant mice. These studies revealed novel pro-inflammatory functions of IL-2 in regulating inflammation in an organ-specific manner. IL-2 exerts its “organ-specific” pro-inflammatory function by regulating the migration and retention of CD4+ T-cells (both Th1 and Th2) specifically to the skin and lung. In addition, IL-2 is also required for regulating the Th2 cytokine response during T-cell activation. Further studies on these IL-2‐regulated genes will help in identifying novel targets for intervention in inflammatory diseases of skin and lung. Both Il2−/− mice and Scurfy (Sf) mutant mice that are deficient in FoxP3, develop multi-organ inflammation but only the latter display severe skin and lung inflammation. In contrast, Sf.Il2−/− double mutant mice do not display skin inflammation and markedly reduced lung inflammation. In this review, we summarize our recent findings based on microarray, q-PCR and functional studies of 10 Sf double mutant mice. These studies revealed novel pro-inflammatory functions of IL-2 in regulating inflammation in an organ-specific manner. IL-2 exerts its “organ-specific” pro-inflammatory function by regulating the migration and retention of CD4+ T-cells (both Th1 and Th2) specifically to the skin and lung. In addition, IL-2 is also required for regulating the Th2 cytokine response during T-cell activation. Further studies on these IL-2‐regulated genes will help in identifying novel targets for intervention in inflammatory diseases of skin and lung. ► IL‐2 is an inflammatory cytokine for skin and lung as well as T‐cell growth. ► Th1 cytokine and related TRGs are insufficient to induce skin and lung inflammation. ► IL‐2 is required for the expression of many of the Th2 related traffic genes. ► IL-2 controls the expression of the adhesion molecule ITGAE, CD103. Both Il2(-/-) mice and Scurfy (Sf) mutant mice that are deficient in FoxP3, develop multi-organ inflammation but only the latter display severe skin and lung inflammation. In contrast, Sf.Il2(-/-) double mutant mice do not display skin inflammation and markedly reduced lung inflammation. In this review, we summarize our recent findings based on microarray, q-PCR and functional studies of 10 Sf double mutant mice. These studies revealed novel pro-inflammatory functions of IL-2 in regulating inflammation in an organ-specific manner. IL-2 exerts its "organ-specific" pro-inflammatory function by regulating the migration and retention of CD4(+) T-cells (both Th1 and Th2) specifically to the skin and lung. In addition, IL-2 is also required for regulating the Th2 cytokine response during T-cell activation. Further studies on these IL-2-regulated genes will help in identifying novel targets for intervention in inflammatory diseases of skin and lung.Both Il2(-/-) mice and Scurfy (Sf) mutant mice that are deficient in FoxP3, develop multi-organ inflammation but only the latter display severe skin and lung inflammation. In contrast, Sf.Il2(-/-) double mutant mice do not display skin inflammation and markedly reduced lung inflammation. In this review, we summarize our recent findings based on microarray, q-PCR and functional studies of 10 Sf double mutant mice. These studies revealed novel pro-inflammatory functions of IL-2 in regulating inflammation in an organ-specific manner. IL-2 exerts its "organ-specific" pro-inflammatory function by regulating the migration and retention of CD4(+) T-cells (both Th1 and Th2) specifically to the skin and lung. In addition, IL-2 is also required for regulating the Th2 cytokine response during T-cell activation. Further studies on these IL-2-regulated genes will help in identifying novel targets for intervention in inflammatory diseases of skin and lung. |
Author | Fu, Shu Man Gaskin, Felicia Sharma, Rahul Ju, Shyr-Te |
AuthorAffiliation | 2 Department of Microbiology, Immunology, and Cancer Biology, University of Virginia, Charlottesville, Virginia, USA 1 Center for Immunity, Inflammation and Regenerative Medicine and Division of Rheumatology and Immunology, Department of Medicine, University of Virginia, Charlottesville, Virginia, USA 3 Department of Psychiatry and Neurobehavioral Sciences, School of Medicine, University of Virginia, Charlottesville, Virginia, USA |
AuthorAffiliation_xml | – name: 3 Department of Psychiatry and Neurobehavioral Sciences, School of Medicine, University of Virginia, Charlottesville, Virginia, USA – name: 1 Center for Immunity, Inflammation and Regenerative Medicine and Division of Rheumatology and Immunology, Department of Medicine, University of Virginia, Charlottesville, Virginia, USA – name: 2 Department of Microbiology, Immunology, and Cancer Biology, University of Virginia, Charlottesville, Virginia, USA |
Author_xml | – sequence: 1 givenname: Shyr-Te surname: Ju fullname: Ju, Shyr-Te organization: Center for Immunity, Inflammation and Regenerative Medicine and Division of Rheumatology and Immunology, Department of Medicine, University of Virginia, Charlottesville, VA, USA – sequence: 2 givenname: Rahul surname: Sharma fullname: Sharma, Rahul organization: Center for Immunity, Inflammation and Regenerative Medicine and Division of Rheumatology and Immunology, Department of Medicine, University of Virginia, Charlottesville, VA, USA – sequence: 3 givenname: Felicia surname: Gaskin fullname: Gaskin, Felicia organization: Department of Psychiatry and Neurobehavioral Sciences, School of Medicine, University of Virginia, Charlottesville, VA, USA – sequence: 4 givenname: Shu Man surname: Fu fullname: Fu, Shu Man email: sf2e@virginia.edu organization: Center for Immunity, Inflammation and Regenerative Medicine and Division of Rheumatology and Immunology, Department of Medicine, University of Virginia, Charlottesville, VA, USA |
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Cites_doi | 10.4049/jimmunol.1002677 10.4049/jimmunol.179.12.8035 10.1038/83707 10.1111/j.1398-9995.2009.02015.x 10.1016/j.jaci.2005.08.046 10.1172/JCI6993 10.1016/j.jaut.2011.01.001 10.1016/0092-8674(93)80067-O 10.1016/S0092-8674(00)80438-9 10.1002/eji.1830251111 10.1038/83784 10.1073/pnas.0400339101 10.4049/jimmunol.136.7.2348 10.1172/JCI40591 10.4049/jimmunol.181.5.3285 10.1093/intimm/12.12.1659 10.1084/jem.187.12.2009 10.1016/j.jaut.2012.02.001 |
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Snippet | Both Il2−/− mice and Scurfy (Sf) mutant mice that are deficient in FoxP3, develop multi-organ inflammation but only the latter display severe skin and lung... Abstract Both Il2 −/− mice and Scurfy (Sf) mutant mice that are deficient in FoxP3, develop multi-organ inflammation but only the latter display severe skin... Both Il2(-/-) mice and Scurfy (Sf) mutant mice that are deficient in FoxP3, develop multi-organ inflammation but only the latter display severe skin and lung... Both Il2-/-mice and Scurfy (Sf) mutant mice that are deficient in FoxP3, develop multi-organ inflammation but only the latter display severe skin and lung... Both Il2 −/− mice and Scurfy (Sf) mutant mice that are deficient in FoxP3, develop multi-organ inflammation but only the latter display severe skin and lung... |
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SubjectTerms | Allergy and Immunology Animals Autoimmune diseases CD4 antigen CD4 Antigens - genetics CD4 Antigens - immunology Cell Movement - genetics Cell Movement - immunology Cytokines - biosynthesis Cytokines - immunology Foxp3 protein Gene expression Gene Expression - immunology Helper cells Inflammation Inflammatory diseases Interleukin 2 Interleukin-2 - genetics Interleukin-2 - immunology Lung Lung - immunology Lung - pathology Lymphocyte Activation - genetics Lymphocyte Activation - immunology Lymphocytes T Mice Mice, Knockout Migration Pneumonia - genetics Pneumonia - immunology Pneumonia - pathology Protein transport Receptors, Cell Surface - genetics Receptors, Cell Surface - immunology Reviews Scurfy mice Skin Skin - immunology Skin - pathology Skin diseases Th1 Cells - immunology Th1 Cells - pathology Th2 Cells - immunology Th2 Cells - pathology Treg |
Title | IL-2 controls trafficking receptor gene expression and Th2 response for skin and lung inflammation |
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