IL-7Rα on CD4+ T cells is required for their survival and the pathogenesis of experimental autoimmune encephalomyelitis

Background The IL-7 receptor alpha (IL-7Rα) binds both IL-7 and thymic stromal lymphopoietin (TSLP). IL-7Rα is essential for the development and survival of naive CD4 + T cells and their differentiation to effector/memory CD4 + T cells. Mice lacking IL-7Rα have severe lymphopenia and are resistant t...

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Published in:	Journal of neuroinflammation Vol. 21; no. 1; pp. 253 - 15
Main Authors:	Azizi, Gholamreza, Van den Broek, Bram, Ishikawa, Larissa Lumi Watanabe, Naziri, Hamed, Yazdani, Reza, Zhang, Guang-Xian, Ciric, Bogoljub, Rostami, Abdolmohamad
Format:	Journal Article
Language:	English
Published:	London BioMed Central 08.10.2024 BMC
Subjects:	Animals Biomedical and Life Sciences Biomedicine CD4+ T cell CD4-Positive T-Lymphocytes - immunology CD4-Positive T-Lymphocytes - metabolism Cell Survival - drug effects Cell Survival - physiology Cytokines - metabolism Encephalomyelitis, Autoimmune, Experimental - chemically induced Encephalomyelitis, Autoimmune, Experimental - genetics Encephalomyelitis, Autoimmune, Experimental - immunology Encephalomyelitis, Autoimmune, Experimental - metabolism Encephalomyelitis, Autoimmune, Experimental - pathology Experimental autoimmune encephalomyelitis IL-7 receptor alpha Immunology Mice Mice, Inbred C57BL Mice, Knockout Mice, Transgenic Multiple sclerosis Myelin-Oligodendrocyte Glycoprotein - immunology Myelin-Oligodendrocyte Glycoprotein - toxicity Neurobiology Neurology Neurosciences Peptide Fragments - immunology Peptide Fragments - metabolism Peptide Fragments - toxicity Receptors, Interleukin-7 - genetics Receptors, Interleukin-7 - metabolism Experimental autoimmune encephalomyelitis Multiple sclerosis CD4 IL-7 receptor alpha T cell CD4+ T cell
ISSN:	1742-2094, 1742-2094
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Abstract	Background The IL-7 receptor alpha (IL-7Rα) binds both IL-7 and thymic stromal lymphopoietin (TSLP). IL-7Rα is essential for the development and survival of naive CD4 + T cells and their differentiation to effector/memory CD4 + T cells. Mice lacking IL-7Rα have severe lymphopenia and are resistant to experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis. However, it has been reported that IL-7Rα on peripheral CD4 + T cells is disposable for their maintenance and EAE pathogenesis, which does not align with the body of knowledge on the role of IL-7Rα in the biology of CD4 + T cells. Given that a definitive study on this important topic is lacking, we revisited it using a novel approach, an inducible knockout of the IL-7Rα gene in CD4 + T cells. Methods We generated Il7ra fl/fl /CD4CreER T2 double transgenic mouse line (henceforth CD4 Δ Il7ra ), susceptible to tamoxifen-induced knockout of the IL-7Rα gene in CD4 + T cells. CD4 Δ Il7ra mice were immunized with MOG 35 − 55 for EAE induction and monitored for disease development. The expression of IL-7Rα, CD4 + T cell numbers, and MOG 35 − 55 -specific CD4 + T cell response was evaluated in the central nervous system (CNS) and lymphoid tissues by flow cytometry. Additionally, splenocytes of CD4 Δ Il7ra mice were stimulated with MOG 35 − 55 to assess their proliferative response and cytokine production by T helper cells. Results Loss of IL-7Rα from the surface of CD4 + T cells in CD4 Δ Il7ra mice was virtually complete several days after tamoxifen treatment. The loss of IL-7Rα in CD4 + T cells led to a gradual and substantial decrease in their numbers in both non-immunized and immunized CD4 Δ Il7ra mice, followed by slow repopulation up to the initial numbers. CD4 Δ Il7ra mice did not develop EAE. We found a decrease in the total numbers of TNF-, IFN-γ-, IL-17 A-, and GM-CSF-producing CD4 + T cells and regulatory T cells in the spleens and CNS of immunized CD4 Δ Il7ra mice. Tracking MOG 35 − 55 -specific CD4 + T cells revealed a significant reduction in their numbers in CD4 Δ Il7ra mice and decreased proliferation and cytokine production in response to MOG 35 − 55 . Conclusion Our study demonstrates that IL-7Rα on peripheral CD4 + T cells is essential for their maintenance, immune response, and EAE pathogenesis.
AbstractList	Abstract Background The IL-7 receptor alpha (IL-7Rα) binds both IL-7 and thymic stromal lymphopoietin (TSLP). IL-7Rα is essential for the development and survival of naive CD4+ T cells and their differentiation to effector/memory CD4+ T cells. Mice lacking IL-7Rα have severe lymphopenia and are resistant to experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis. However, it has been reported that IL-7Rα on peripheral CD4+ T cells is disposable for their maintenance and EAE pathogenesis, which does not align with the body of knowledge on the role of IL-7Rα in the biology of CD4+ T cells. Given that a definitive study on this important topic is lacking, we revisited it using a novel approach, an inducible knockout of the IL-7Rα gene in CD4+ T cells. Methods We generated Il7ra fl/fl/CD4CreERT2 double transgenic mouse line (henceforth CD4ΔIl7ra ), susceptible to tamoxifen-induced knockout of the IL-7Rα gene in CD4+ T cells. CD4ΔIl7ra mice were immunized with MOG35 − 55 for EAE induction and monitored for disease development. The expression of IL-7Rα, CD4+ T cell numbers, and MOG35 − 55-specific CD4+ T cell response was evaluated in the central nervous system (CNS) and lymphoid tissues by flow cytometry. Additionally, splenocytes of CD4ΔIl7ra mice were stimulated with MOG35 − 55 to assess their proliferative response and cytokine production by T helper cells. Results Loss of IL-7Rα from the surface of CD4+ T cells in CD4ΔIl7ra mice was virtually complete several days after tamoxifen treatment. The loss of IL-7Rα in CD4+ T cells led to a gradual and substantial decrease in their numbers in both non-immunized and immunized CD4ΔIl7ra mice, followed by slow repopulation up to the initial numbers. CD4ΔIl7ra mice did not develop EAE. We found a decrease in the total numbers of TNF-, IFN-γ-, IL-17 A-, and GM-CSF-producing CD4+ T cells and regulatory T cells in the spleens and CNS of immunized CD4ΔIl7ra mice. Tracking MOG35 − 55-specific CD4+ T cells revealed a significant reduction in their numbers in CD4ΔIl7ra mice and decreased proliferation and cytokine production in response to MOG35 − 55. Conclusion Our study demonstrates that IL-7Rα on peripheral CD4+ T cells is essential for their maintenance, immune response, and EAE pathogenesis. The IL-7 receptor alpha (IL-7Rα) binds both IL-7 and thymic stromal lymphopoietin (TSLP). IL-7Rα is essential for the development and survival of naive CD4 T cells and their differentiation to effector/memory CD4 T cells. Mice lacking IL-7Rα have severe lymphopenia and are resistant to experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis. However, it has been reported that IL-7Rα on peripheral CD4 T cells is disposable for their maintenance and EAE pathogenesis, which does not align with the body of knowledge on the role of IL-7Rα in the biology of CD4 T cells. Given that a definitive study on this important topic is lacking, we revisited it using a novel approach, an inducible knockout of the IL-7Rα gene in CD4 T cells. We generated Il7ra /CD4CreER double transgenic mouse line (henceforth CD4 ), susceptible to tamoxifen-induced knockout of the IL-7Rα gene in CD4 T cells. CD4 mice were immunized with MOG for EAE induction and monitored for disease development. The expression of IL-7Rα, CD4 T cell numbers, and MOG -specific CD4 T cell response was evaluated in the central nervous system (CNS) and lymphoid tissues by flow cytometry. Additionally, splenocytes of CD4 mice were stimulated with MOG to assess their proliferative response and cytokine production by T helper cells. Loss of IL-7Rα from the surface of CD4 T cells in CD4 mice was virtually complete several days after tamoxifen treatment. The loss of IL-7Rα in CD4 T cells led to a gradual and substantial decrease in their numbers in both non-immunized and immunized CD4 mice, followed by slow repopulation up to the initial numbers. CD4 mice did not develop EAE. We found a decrease in the total numbers of TNF-, IFN-γ-, IL-17 A-, and GM-CSF-producing CD4 T cells and regulatory T cells in the spleens and CNS of immunized CD4 mice. Tracking MOG -specific CD4 T cells revealed a significant reduction in their numbers in CD4 mice and decreased proliferation and cytokine production in response to MOG . Our study demonstrates that IL-7Rα on peripheral CD4 T cells is essential for their maintenance, immune response, and EAE pathogenesis. The IL-7 receptor alpha (IL-7Rα) binds both IL-7 and thymic stromal lymphopoietin (TSLP). IL-7Rα is essential for the development and survival of naive CD4+ T cells and their differentiation to effector/memory CD4+ T cells. Mice lacking IL-7Rα have severe lymphopenia and are resistant to experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis. However, it has been reported that IL-7Rα on peripheral CD4+ T cells is disposable for their maintenance and EAE pathogenesis, which does not align with the body of knowledge on the role of IL-7Rα in the biology of CD4+ T cells. Given that a definitive study on this important topic is lacking, we revisited it using a novel approach, an inducible knockout of the IL-7Rα gene in CD4+ T cells.BACKGROUNDThe IL-7 receptor alpha (IL-7Rα) binds both IL-7 and thymic stromal lymphopoietin (TSLP). IL-7Rα is essential for the development and survival of naive CD4+ T cells and their differentiation to effector/memory CD4+ T cells. Mice lacking IL-7Rα have severe lymphopenia and are resistant to experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis. However, it has been reported that IL-7Rα on peripheral CD4+ T cells is disposable for their maintenance and EAE pathogenesis, which does not align with the body of knowledge on the role of IL-7Rα in the biology of CD4+ T cells. Given that a definitive study on this important topic is lacking, we revisited it using a novel approach, an inducible knockout of the IL-7Rα gene in CD4+ T cells.We generated Il7rafl/fl/CD4CreERT2 double transgenic mouse line (henceforth CD4ΔIl7ra), susceptible to tamoxifen-induced knockout of the IL-7Rα gene in CD4+ T cells. CD4ΔIl7ra mice were immunized with MOG35 - 55 for EAE induction and monitored for disease development. The expression of IL-7Rα, CD4+ T cell numbers, and MOG35 - 55-specific CD4+ T cell response was evaluated in the central nervous system (CNS) and lymphoid tissues by flow cytometry. Additionally, splenocytes of CD4ΔIl7ra mice were stimulated with MOG35 - 55 to assess their proliferative response and cytokine production by T helper cells.METHODSWe generated Il7rafl/fl/CD4CreERT2 double transgenic mouse line (henceforth CD4ΔIl7ra), susceptible to tamoxifen-induced knockout of the IL-7Rα gene in CD4+ T cells. CD4ΔIl7ra mice were immunized with MOG35 - 55 for EAE induction and monitored for disease development. The expression of IL-7Rα, CD4+ T cell numbers, and MOG35 - 55-specific CD4+ T cell response was evaluated in the central nervous system (CNS) and lymphoid tissues by flow cytometry. Additionally, splenocytes of CD4ΔIl7ra mice were stimulated with MOG35 - 55 to assess their proliferative response and cytokine production by T helper cells.Loss of IL-7Rα from the surface of CD4+ T cells in CD4ΔIl7ra mice was virtually complete several days after tamoxifen treatment. The loss of IL-7Rα in CD4+ T cells led to a gradual and substantial decrease in their numbers in both non-immunized and immunized CD4ΔIl7ra mice, followed by slow repopulation up to the initial numbers. CD4ΔIl7ra mice did not develop EAE. We found a decrease in the total numbers of TNF-, IFN-γ-, IL-17 A-, and GM-CSF-producing CD4+ T cells and regulatory T cells in the spleens and CNS of immunized CD4ΔIl7ra mice. Tracking MOG35 - 55-specific CD4+ T cells revealed a significant reduction in their numbers in CD4ΔIl7ra mice and decreased proliferation and cytokine production in response to MOG35 - 55.RESULTSLoss of IL-7Rα from the surface of CD4+ T cells in CD4ΔIl7ra mice was virtually complete several days after tamoxifen treatment. The loss of IL-7Rα in CD4+ T cells led to a gradual and substantial decrease in their numbers in both non-immunized and immunized CD4ΔIl7ra mice, followed by slow repopulation up to the initial numbers. CD4ΔIl7ra mice did not develop EAE. We found a decrease in the total numbers of TNF-, IFN-γ-, IL-17 A-, and GM-CSF-producing CD4+ T cells and regulatory T cells in the spleens and CNS of immunized CD4ΔIl7ra mice. Tracking MOG35 - 55-specific CD4+ T cells revealed a significant reduction in their numbers in CD4ΔIl7ra mice and decreased proliferation and cytokine production in response to MOG35 - 55.Our study demonstrates that IL-7Rα on peripheral CD4+ T cells is essential for their maintenance, immune response, and EAE pathogenesis.CONCLUSIONOur study demonstrates that IL-7Rα on peripheral CD4+ T cells is essential for their maintenance, immune response, and EAE pathogenesis. Background The IL-7 receptor alpha (IL-7Rα) binds both IL-7 and thymic stromal lymphopoietin (TSLP). IL-7Rα is essential for the development and survival of naive CD4 + T cells and their differentiation to effector/memory CD4 + T cells. Mice lacking IL-7Rα have severe lymphopenia and are resistant to experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis. However, it has been reported that IL-7Rα on peripheral CD4 + T cells is disposable for their maintenance and EAE pathogenesis, which does not align with the body of knowledge on the role of IL-7Rα in the biology of CD4 + T cells. Given that a definitive study on this important topic is lacking, we revisited it using a novel approach, an inducible knockout of the IL-7Rα gene in CD4 + T cells. Methods We generated Il7ra fl/fl /CD4CreER T2 double transgenic mouse line (henceforth CD4 Δ Il7ra ), susceptible to tamoxifen-induced knockout of the IL-7Rα gene in CD4 + T cells. CD4 Δ Il7ra mice were immunized with MOG 35 − 55 for EAE induction and monitored for disease development. The expression of IL-7Rα, CD4 + T cell numbers, and MOG 35 − 55 -specific CD4 + T cell response was evaluated in the central nervous system (CNS) and lymphoid tissues by flow cytometry. Additionally, splenocytes of CD4 Δ Il7ra mice were stimulated with MOG 35 − 55 to assess their proliferative response and cytokine production by T helper cells. Results Loss of IL-7Rα from the surface of CD4 + T cells in CD4 Δ Il7ra mice was virtually complete several days after tamoxifen treatment. The loss of IL-7Rα in CD4 + T cells led to a gradual and substantial decrease in their numbers in both non-immunized and immunized CD4 Δ Il7ra mice, followed by slow repopulation up to the initial numbers. CD4 Δ Il7ra mice did not develop EAE. We found a decrease in the total numbers of TNF-, IFN-γ-, IL-17 A-, and GM-CSF-producing CD4 + T cells and regulatory T cells in the spleens and CNS of immunized CD4 Δ Il7ra mice. Tracking MOG 35 − 55 -specific CD4 + T cells revealed a significant reduction in their numbers in CD4 Δ Il7ra mice and decreased proliferation and cytokine production in response to MOG 35 − 55 . Conclusion Our study demonstrates that IL-7Rα on peripheral CD4 + T cells is essential for their maintenance, immune response, and EAE pathogenesis.
ArticleNumber	253
Author	Van den Broek, Bram Ciric, Bogoljub Zhang, Guang-Xian Ishikawa, Larissa Lumi Watanabe Naziri, Hamed Rostami, Abdolmohamad Azizi, Gholamreza Yazdani, Reza
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Snippet	Background The IL-7 receptor alpha (IL-7Rα) binds both IL-7 and thymic stromal lymphopoietin (TSLP). IL-7Rα is essential for the development and survival of... The IL-7 receptor alpha (IL-7Rα) binds both IL-7 and thymic stromal lymphopoietin (TSLP). IL-7Rα is essential for the development and survival of naive CD4 T... The IL-7 receptor alpha (IL-7Rα) binds both IL-7 and thymic stromal lymphopoietin (TSLP). IL-7Rα is essential for the development and survival of naive CD4+ T... Abstract Background The IL-7 receptor alpha (IL-7Rα) binds both IL-7 and thymic stromal lymphopoietin (TSLP). IL-7Rα is essential for the development and...
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SubjectTerms	Animals Biomedical and Life Sciences Biomedicine CD4+ T cell CD4-Positive T-Lymphocytes - immunology CD4-Positive T-Lymphocytes - metabolism Cell Survival - drug effects Cell Survival - physiology Cytokines - metabolism Encephalomyelitis, Autoimmune, Experimental - chemically induced Encephalomyelitis, Autoimmune, Experimental - genetics Encephalomyelitis, Autoimmune, Experimental - immunology Encephalomyelitis, Autoimmune, Experimental - metabolism Encephalomyelitis, Autoimmune, Experimental - pathology Experimental autoimmune encephalomyelitis IL-7 receptor alpha Immunology Mice Mice, Inbred C57BL Mice, Knockout Mice, Transgenic Multiple sclerosis Myelin-Oligodendrocyte Glycoprotein - immunology Myelin-Oligodendrocyte Glycoprotein - toxicity Neurobiology Neurology Neurosciences Peptide Fragments - immunology Peptide Fragments - metabolism Peptide Fragments - toxicity Receptors, Interleukin-7 - genetics Receptors, Interleukin-7 - metabolism
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Title	IL-7Rα on CD4+ T cells is required for their survival and the pathogenesis of experimental autoimmune encephalomyelitis
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