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Mechanism underlying polyvalent IgG-induced regulatory T cell activation and its clinical application: Anti-idiotypic regulatory T cell theory for immune tolerance

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dc.contributor.authorVictor, JR-
dc.contributor.authorNahm, DH-
dc.date.accessioned2024-01-23T07:54:39Z-
dc.date.available2024-01-23T07:54:39Z-
dc.date.issued2023-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/32122-
dc.description.abstractThe regulatory T (Treg) cells constitute a functionally defined subpopulation of T cells that modulate the immune system and maintain immune tolerance through suppression of the development of autoimmune responses to self-antigens and allergic reactions to external antigens. Reduction in the number or function of Treg cells has been suggested as a key immune abnormality underlying the development of autoimmune and allergic diseases. In vitro studies have demonstrated that purified polyvalent immunoglobulin G (IgG) from multiple healthy blood donors can exert immunomodulatory effects on Treg cells. Incubation of polyvalent human IgG with purified CD4+CD25high T cells increased the intracellular expression of interleukin (IL)-10. Intravenous administration of polyvalent human IgG induced significant expansions of CD4+ Foxp3+ Treg cells and clinical improvements in patients with autoimmune diseases. In human clinical trials, intramuscular administration of autologous total IgG significantly increased the percentage of IL-10-producing CD4+ Treg cells in the peripheral blood of healthy subjects and provided significant clinical improvements in patients with atopic dermatitis. These results suggest a clinical usefulness of polyvalent IgG-induced activation of Treg cells in human subjects. This review proposes a new hypothesis for immune tolerance mechanism by integrating the pre-existing “idiotypic network theory” and “Treg cell theory” into an “anti-idiotypic Treg cell theory.” Based on this hypothesis, an “active anti-idiotypic therapy” for allergic and autoimmune diseases using autologous polyvalent IgG (as immunizing antigens) is suggested as follows: (1) Intramuscular or subcutaneous administration of autologous polyvalent IgG produces numerous immunogenic peptides derived from idiotypes of autologous IgG through processing of dendritic cells, and these peptides activate anti-idiotypic Treg cells in the same subject. (2) Activated anti-idiotypic Treg cells secrete IL-10 and suppress Th2 cell response to allergens and autoimmune T cell response to self-antigens. (3) These events can induce a long-term clinical improvements in patients with allergic and autoimmune diseases. Further studies are needed to evaluate the detailed molecular mechanism underlying polyvalent IgG-induced Treg cell activation and the clinical usefulness of this immunomodulatory therapy for autoimmune and allergic diseases.-
dc.language.isoen-
dc.subject.MESHAllergens-
dc.subject.MESHAutoantigens-
dc.subject.MESHAutoimmune Diseases-
dc.subject.MESHHumans-
dc.subject.MESHHypersensitivity-
dc.subject.MESHImmune Tolerance-
dc.subject.MESHImmunoglobulin G-
dc.subject.MESHInterleukin-10-
dc.subject.MESHT-Lymphocytes, Regulatory-
dc.titleMechanism underlying polyvalent IgG-induced regulatory T cell activation and its clinical application: Anti-idiotypic regulatory T cell theory for immune tolerance-
dc.typeArticle-
dc.identifier.pmid38094290-
dc.identifier.urlhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10716439-
dc.subject.keywordallergic disease-
dc.subject.keywordatopic dermatitis-
dc.subject.keywordautoimmune disease-
dc.subject.keywordimmune tolerance-
dc.subject.keywordimmunoglobulins-
dc.subject.keywordimmunomodulation-
dc.subject.keywordregulatory T cell-
dc.subject.keywordT-lymphocytes-
dc.contributor.affiliatedAuthorNahm, DH-
dc.type.localJournal Papers-
dc.identifier.doi10.3389/fimmu.2023.1242860-
dc.citation.titleFrontiers in immunology-
dc.citation.volume14-
dc.citation.date2023-
dc.citation.startPage1242860-
dc.citation.endPage1242860-
dc.identifier.bibliographicCitationFrontiers in immunology, 14. : 1242860-1242860, 2023-
dc.identifier.eissn1664-3224-
dc.relation.journalidJ016643224-
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Journal Papers > School of Medicine / Graduate School of Medicine > Allergy
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