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 inClinical immunology (Orlando, Fla.) Vol. 145; no. 1; pp. 82 - 88
Main Authors Ju, Shyr-Te, Sharma, Rahul, Gaskin, Felicia, Fu, Shu Man
Format Journal Article
LanguageEnglish
Published United States 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.
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
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Keywords Inflammation
Scurfy mice
Autoimmune diseases
MOI
Treg
Multi-organ inflammation
Language English
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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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StartPage 82
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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https://dx.doi.org/10.1016/j.clim.2012.07.015
https://www.ncbi.nlm.nih.gov/pubmed/22940635
https://www.proquest.com/docview/1041002256
https://www.proquest.com/docview/1093467092
https://pubmed.ncbi.nlm.nih.gov/PMC3444569
Volume 145
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