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Failure of iNature immune regulation can lead to autoimmune diseases.
It has been recognized that regulatory T cells (Tregs) are essential to ensure immune homeostasis through their ability to induce and maintain immune tolerance.
However, experimental and clinical efforts to use non-specific Tregs to treat autoimmune diseases may increase the risk of systemic immunosuppression in patients.
Inducing antigen-specific immune tolerance in a dysregulated immune system is a challenge.
On March 10, 2021, Jin Yan, Shiyu Liu of the Air Force Military Medical University and Chen Xin of Xi’an Jiaotong University jointly published an online communication titled "Modular immune-homeostatic microparticles promote immune tolerance in mouse autoimmune models" in Science Translational Medicine (IF=16) The research paper developed the immune homeostasis microparticles (IHM), which can treat a variety of mouse autoimmune models by inducing the apoptosis of activated T cells and rebuilding regulatory T cells.
Specifically, in the experimental model of colitis, IHM rapidly releases monocyte chemoattractant protein-1 after intravenous administration, which recruits activated T cells and then induces their apoptosis through Fas ligand on the surface of IHM.
Die.
This triggers macrophages to take up apoptotic T cells and produce a large amount of transforming growth factor-β, thereby promoting the differentiation of regulatory T cells.
In addition, the modular design of IHM allows IHM to be engineered with self-antigen peptides, which can reduce disease in experimental autoimmune encephalomyelitis mouse models and non-obese diabetic mouse models.
This is achieved by inducing T cell apoptosis and the sustained release of autoantigens after the production of macrophage transforming growth factor-β, thereby promoting the establishment of an immune tolerance environment.
Therefore, by inducing apoptosis and re-establishing a tolerant immune response, IHMs may be an effective treatment strategy for autoimmune diseases.
Failure of immune regulation can lead to autoimmune diseases.
It has been recognized that regulatory T cells (Tregs) are essential to ensure immune homeostasis through their ability to induce and maintain immune tolerance.
However, experimental and clinical efforts to use non-specific Tregs to treat autoimmune diseases may increase the risk of systemic immunosuppression in patients.
In order to overcome these obstacles, several methods have been reported that focus on the generation of antigen-specific Tregs that inhibit inflammatory pathogenesis and autoimmunity without compromising the overall immune response, including the administration of autoantigens during T cell initiation.
Although these methods have shown efficacy in experimental animal models of autoimmunity and chronic inflammation, their significant therapeutic effects on human diseases have not yet been reported.
This may be attributed to the fact that in clinical transformation, it is difficult to produce long-term immune tolerance in the case of an established autoimmune disease patient's immune system dysregulation.
Some clinical studies have shown that it is necessary to destroy the dysregulated immune response before resetting the patient's immune system.
It has been proposed that in an established autoimmune disease state, Tregs may lose their immunosuppressive function and transform into pro-inflammatory T effector cells, such as T helper cells 17 (TH17).
Therefore, patients may experience recurrence of the disease.
Therefore, destroying the inflammatory immune response that drives autoimmunity before rebuilding a balanced immune system represents a reasonable strategy for the development of antigen-specific immunotherapy.
Strategies used so far to disrupt the dysregulated immune response, such as radiation and antibodies, may also increase the risk of widespread off-target effects on the immune system, leading to immunodeficiency.
In addition, the effective induction of antigen-specific immune tolerance requires precise coordination of T cell programming, which is difficult to achieve.
Recently, biomaterials functionalized with various specific molecules have been explored for precise regulation of cell behavior, such as apoptosis, differentiation, and migration.
This biological material can be used as an immunomodulator.
Researchers have reported the tolerance effect of autoimmune disease-related peptides with microparticles used in mice with experimental autoimmune encephalomyelitis (EAE).
Or nanoparticles.
This strategy provides a strategy for performing sequential deletion of the dysfunctional immune system and then inducing antigen-specific immune tolerance.
Here, the study demonstrated the potential of modular immune homeostasis particles (IHMs) to promote immune tolerance in a variety of autoimmune mouse models.
Specifically, in the experimental model of colitis, IHM rapidly releases monocyte chemoattractant protein-1 after intravenous administration.
This protein recruits activated T cells and then induces their apoptosis through Fas ligand on the surface of IHM.
Die.
This triggers macrophages to take up apoptotic T cells and produce a large amount of transforming growth factor-β, thereby promoting the differentiation of regulatory T cells.
In addition, the modular design of IHM allows IHM to be engineered with self-antigen peptides, which can reduce disease in experimental autoimmune encephalomyelitis mouse models and non-obese diabetic mouse models.
This is achieved by inducing T cell apoptosis and the sustained release of autoantigens after the production of macrophage transforming growth factor-β, thereby promoting the establishment of an immune tolerance environment.
Therefore, by inducing apoptosis and re-establishing tolerant immune response, IHMs may be an effective treatment strategy for autoimmune diseases.
Reference message: https://stm.
sciencemag.
org/content/13/584/eaaw9668
It has been recognized that regulatory T cells (Tregs) are essential to ensure immune homeostasis through their ability to induce and maintain immune tolerance.
However, experimental and clinical efforts to use non-specific Tregs to treat autoimmune diseases may increase the risk of systemic immunosuppression in patients.
Inducing antigen-specific immune tolerance in a dysregulated immune system is a challenge.
On March 10, 2021, Jin Yan, Shiyu Liu of the Air Force Military Medical University and Chen Xin of Xi’an Jiaotong University jointly published an online communication titled "Modular immune-homeostatic microparticles promote immune tolerance in mouse autoimmune models" in Science Translational Medicine (IF=16) The research paper developed the immune homeostasis microparticles (IHM), which can treat a variety of mouse autoimmune models by inducing the apoptosis of activated T cells and rebuilding regulatory T cells.
Specifically, in the experimental model of colitis, IHM rapidly releases monocyte chemoattractant protein-1 after intravenous administration, which recruits activated T cells and then induces their apoptosis through Fas ligand on the surface of IHM.
Die.
This triggers macrophages to take up apoptotic T cells and produce a large amount of transforming growth factor-β, thereby promoting the differentiation of regulatory T cells.
In addition, the modular design of IHM allows IHM to be engineered with self-antigen peptides, which can reduce disease in experimental autoimmune encephalomyelitis mouse models and non-obese diabetic mouse models.
This is achieved by inducing T cell apoptosis and the sustained release of autoantigens after the production of macrophage transforming growth factor-β, thereby promoting the establishment of an immune tolerance environment.
Therefore, by inducing apoptosis and re-establishing a tolerant immune response, IHMs may be an effective treatment strategy for autoimmune diseases.
Failure of immune regulation can lead to autoimmune diseases.
It has been recognized that regulatory T cells (Tregs) are essential to ensure immune homeostasis through their ability to induce and maintain immune tolerance.
However, experimental and clinical efforts to use non-specific Tregs to treat autoimmune diseases may increase the risk of systemic immunosuppression in patients.
In order to overcome these obstacles, several methods have been reported that focus on the generation of antigen-specific Tregs that inhibit inflammatory pathogenesis and autoimmunity without compromising the overall immune response, including the administration of autoantigens during T cell initiation.
Although these methods have shown efficacy in experimental animal models of autoimmunity and chronic inflammation, their significant therapeutic effects on human diseases have not yet been reported.
This may be attributed to the fact that in clinical transformation, it is difficult to produce long-term immune tolerance in the case of an established autoimmune disease patient's immune system dysregulation.
Some clinical studies have shown that it is necessary to destroy the dysregulated immune response before resetting the patient's immune system.
It has been proposed that in an established autoimmune disease state, Tregs may lose their immunosuppressive function and transform into pro-inflammatory T effector cells, such as T helper cells 17 (TH17).
Therefore, patients may experience recurrence of the disease.
Therefore, destroying the inflammatory immune response that drives autoimmunity before rebuilding a balanced immune system represents a reasonable strategy for the development of antigen-specific immunotherapy.
Strategies used so far to disrupt the dysregulated immune response, such as radiation and antibodies, may also increase the risk of widespread off-target effects on the immune system, leading to immunodeficiency.
In addition, the effective induction of antigen-specific immune tolerance requires precise coordination of T cell programming, which is difficult to achieve.
Recently, biomaterials functionalized with various specific molecules have been explored for precise regulation of cell behavior, such as apoptosis, differentiation, and migration.
This biological material can be used as an immunomodulator.
Researchers have reported the tolerance effect of autoimmune disease-related peptides with microparticles used in mice with experimental autoimmune encephalomyelitis (EAE).
Or nanoparticles.
This strategy provides a strategy for performing sequential deletion of the dysfunctional immune system and then inducing antigen-specific immune tolerance.
Here, the study demonstrated the potential of modular immune homeostasis particles (IHMs) to promote immune tolerance in a variety of autoimmune mouse models.
Specifically, in the experimental model of colitis, IHM rapidly releases monocyte chemoattractant protein-1 after intravenous administration.
This protein recruits activated T cells and then induces their apoptosis through Fas ligand on the surface of IHM.
Die.
This triggers macrophages to take up apoptotic T cells and produce a large amount of transforming growth factor-β, thereby promoting the differentiation of regulatory T cells.
In addition, the modular design of IHM allows IHM to be engineered with self-antigen peptides, which can reduce disease in experimental autoimmune encephalomyelitis mouse models and non-obese diabetic mouse models.
This is achieved by inducing T cell apoptosis and the sustained release of autoantigens after the production of macrophage transforming growth factor-β, thereby promoting the establishment of an immune tolerance environment.
Therefore, by inducing apoptosis and re-establishing tolerant immune response, IHMs may be an effective treatment strategy for autoimmune diseases.
Reference message: https://stm.
sciencemag.
org/content/13/584/eaaw9668
