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Title: | Treg enhancing therapies to treat autoimmune diseases. | Authors: | Ooi J.D.;Eggenhuizen P.J.;Ng B.H. | Institution: | (Eggenhuizen, Ng, Ooi) Centre for Inflammatory Diseases, Monash University, Department of Medicine, Monash Medical Centre, Clayton, VIC 3168, Australia | Issue Date: | 9-Nov-2020 | Copyright year: | 2020 | Publisher: | MDPI AG (E-mail: diversity@mdpi.com) | Place of publication: | Switzerland | Publication information: | International Journal of Molecular Sciences. 21 (19) (pp 1-18), 2020. Article Number: 7015. Date of Publication: 01 Oct 2020. | Journal: | International Journal of Molecular Sciences | Abstract: | Regulatory T cells (Tregs) are a small yet critical subset of CD4+ T cells, which have the role of maintaining immune homeostasis by, for example, regulating self-tolerance, tumor immunity, anti-microbial resistance, allergy and transplantation rejection. The suppressive mechanisms by which Tregs function are varied and pleiotropic. The ability of Tregs to maintain self-tolerance means they are critical for the control and prevention of autoimmune diseases. Irregularities in Treg function and number can result in loss of tolerance and autoimmune disease. Restoring immune homeostasis and tolerance through the promotion, activation or delivery of Tregs has emerged as a focus for therapies aimed at curing or controlling autoimmune diseases. Such therapies have focused on the Treg cell subset by using drugs to suppress T effector cells and promote Tregs. Other approaches have trialed inducing tolerance by administering the autoantigen via direct administration, by transient expression using a DNA vector, or by antigen-specific nanoparticles. More recently, cell-based therapies have been developed as an approach to directly or indirectly enhance Treg cell specificity, function and number. This can be achieved indirectly by transfer of tolerogenic dendritic cells, which have the potential to expand antigen-specific Treg cells. Treg cells can be directly administered to treat autoimmune disease by way of polyclonal Tregs or Tregs transduced with a receptor with high affinity for the target autoantigen, such as a high affinity T cell receptor (TCR) or a chimeric antigen receptor (CAR). This review will discuss the strategies being developed to redirect autoimmune responses to a state of immune tolerance, with the aim of the prevention or amelioration of autoimmune disease.Copyright © 2020 by the authors. Licensee MDPI, Basel, Switzerland. | DOI: | http://monash.idm.oclc.org/login?url=http://dx.doi.org/10.3390/ijms21197015 | PubMed URL: | 32977677 [http://www.ncbi.nlm.nih.gov/pubmed/?term=32977677] | ISSN: | 1661-6596 | URI: | https://repository.monashhealth.org/monashhealthjspui/handle/1/29021 | Type: | Review | Subjects: | Crohn disease/th [Therapy] dendritic cell DNA immunization DNA vector drug targeting effector cell fecal microbiota transplantation graft rejection immunological tolerance insulin dependent diabetes mellitus/dt [Drug Therapy] insulin dependent diabetes mellitus/et [Etiology] low drug dose microbiome multiple sclerosis/et [Etiology] nonhuman pemphigus/th [Therapy] phenotype *regulatory T lymphocyte review skin lupus erythematosus/th [Therapy] synergistic effect systemic lupus erythematosus/et [Etiology] T lymphocyte subpopulation transient expression treatment outcome umbilical cord blood aldesleukin/dt [Drug Therapy] autoantigen bacterial polysaccharide beta glucan butyric acid CD135 antigen *chimeric antigen receptor/ec [Endogenous Compound] corticosteroid/dt [Drug Therapy] cytokine receptor agonist/dt [Drug Therapy] cytokine receptor agonist/pd [Pharmacology] cytotoxic T lymphocyte antigen 4/ec [Endogenous Compound] Flt3 ligand/cb [Drug Combination] Flt3 ligand/it [Drug Interaction] Flt3 ligand/dt [Drug Therapy] galactan immunosuppressive agent/dt [Drug Therapy] insulin/dt [Drug Therapy] interleukin 10/dt [Drug Therapy] interleukin 10/pd [Pharmacology] major histocompatibility antigen/ec [Endogenous Compound] mammalian target of rapamycin/ec [Endogenous Compound] mammalian target of rapamycin inhibitor/dt [Drug Therapy] mammalian target of rapamycin inhibitor/pd [Pharmacology] methylprednisolone/do [Drug Dose] methylprednisolone/dt [Drug Therapy] mycophenolic acid/do [Drug Dose] mycophenolic acid/dt [Drug Therapy] nanoparticle peptide/dt [Drug Therapy] rapamycin/cb [Drug Combination] rapamycin/it [Drug Interaction] rapamycin/dt [Drug Therapy] rapamycin/pd [Pharmacology] recombinant interleukin 2/do [Drug Dose] recombinant interleukin 2/dt [Drug Therapy] short chain fatty acid *T lymphocyte receptor/ec [Endogenous Compound] tacrolimus/do [Drug Dose] tacrolimus/dt [Drug Therapy] transcription factor FOXP3/ec [Endogenous Compound] tumor necrosis factor receptor 2/ec [Endogenous Compound] unclassified drug tumor necrosis factor receptor 2 agonist/dt [Drug Therapy] tumor necrosis factor receptor 2 agonist/pd [Pharmacology] human adverse event antigen specificity antiinflammatory activity *autoimmune disease/dt [Drug Therapy] *autoimmune disease/et [Etiology] *autoimmune disease/pc [Prevention] *autoimmune disease/th [Therapy] autoimmune hepatitis/th [Therapy] autoimmunity Bifidobacterium bifidum biological therapy CD4+ T lymphocyte cell therapy *chimeric antigen receptor immunotherapy chronic inflammation *chimeric antigen receptor immunotherapy chronic inflammation Crohn disease / therapy dendritic cell DNA immunization DNA vector drug targeting effector cell fecal microbiota transplantation graft rejection human immunological tolerance insulin dependent diabetes mellitus / drug therapy / etiology low drug dose microbiome multiple sclerosis / etiology nonhuman pemphigus / therapy phenotype *regulatory T lymphocyte Review skin lupus erythematosus / therapy synergistic effect antigen specificity T lymphocyte subpopulation transient expression treatment outcome umbilical cord blood adverse event systemic lupus erythematosus / etiology antiinflammatory activity *autoimmune disease / *drug therapy / *etiology / *prevention / *therapy autoimmune hepatitis / therapy autoimmunity Bifidobacterium bifidum biological therapy CD4+ T lymphocyte cell therapy |
Type of Clinical Study or Trial: | Review article (e.g. literature review, narrative review) |
Appears in Collections: | Articles |
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