Background: Systemic lupus erythematosus (SLE) is a complex autoimmune disease that affects multiple organ systems. A key element in maintaining immune tolerance and preventing autoimmunity is the role of regulatory T cells (Treg cells). Among these, HLA-DR Treg cells represent a distinct subset, and their altered expression and functionality in SLE are closely associated with the progression of the disease. This review explores the biological characteristics of HLA-DR Treg cells, their mechanisms of action in SLE, as well as their potential and the challenges they pose as therapeutic targets.
Methods And Results: This review offers a comprehensive analysis of the mechanisms by which HLA-DR Treg cells regulate immune responses. It highlights their direct interactions with autoreactive T cells and antigen-presenting cells, which contribute to the suppression of autoimmunity. Additionally, the review explores the critical role of these cells in maintaining immune tolerance and their promising potential in the context of antigen-specific immunotherapy.
Discussion: The potential of HLA-DR Treg cells in the treatment of systemic lupus erythematosus (SLE) is considerable, particularly due to their capacity to generate antigen-specific Tregs. The development of Treg-based therapies, including the expansion of both polyclonal and antigen-specific Tregs, is an area of active investigation. Nonetheless, several challenges persist, such as the need to optimize protocols for Treg generation and expansion, ensure the stability of the Treg phenotype, and address potential safety concerns associated with cellular therapies.Continued research is essential to fully harness the potential of HLA-DR Treg cells in the treatment of SLE and other autoimmune diseases.
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http://dx.doi.org/10.1080/08820139.2025.2475816 | DOI Listing |
J Immunol
January 2025
Institute of Microbiology and Immunology, National Yang Ming Chiao Tung University, Taipei City, Taiwan.
Decoy receptor 3 (DcR3), a soluble receptor in the tumor necrosis factor receptor superfamily, regulates the functions of monocytes, macrophages, dendritic cells, and T cells. Previous studies have demonstrated that DcR3 suppresses B cell proliferation in vitro and ameliorates autoimmune diseases in animal models; however, whether and how DcR3 regulates antibody production is unclear. Using a DcR3 transgenic mouse model, we found that DcR3 impaired the T cell-dependent antigen-stimulated antibody response.
View Article and Find Full Text PDFJ Immunol
February 2025
Genentech, Inc, South San Francisco, CA, United States.
A gene encoding the transcription factor RTF1 has been associated with an increased risk of ulcerative colitis (UC). In this study, we investigated its function in modulating T cells expressing interleukin-17A (Th17 cells), a cardinal cell type promoting intestinal inflammation. Our results indicate that Rtf1 deficiency disrupts the differentiation of Th17 cells, while leaving regulatory T cells (Treg) unaffected.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
March 2025
Division of Immunobiology, Institute for Genetic Medicine, Hokkaido University, Sapporo, Hokkaido 060-0815, Japan.
Currently, most cell or tissue transplantations using induced pluripotent stem cells (iPSCs) are anticipated to involve allogeneic iPSCs. However, the immunological properties of iPSCs in an allogeneic setting are not well understood. We previously established a mouse transplantation model of MHC-compatible/minor antigen-mismatched combinations, assuming a hypoimmunogenic iPSC-setting.
View Article and Find Full Text PDFJ Int Med Res
March 2025
Infectious Diseases and Clinical Microbiology Clinic, University of Health Science Izmir Bozyaka Training and Research Hospital, Izmir, Turkey.
ObjectivesAcute leukemia often leads to severe complications such as febrile neutropenia. Mortality rates remain high, underscoring the need for novel prognostic markers. Regulatory T cells (Tregs) have not been extensively studied in this context.
View Article and Find Full Text PDFRheumatology (Oxford)
March 2025
Vasculitis Expertise Center, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
In this plenary session of the Vasculitis Workshop 2024, pioneering translational research on autoimmune vasculitis, particularly ANCA-associated vasculitis (AAV), was presented, highlighting advancements in our understanding of disease mechanisms and promising therapeutic prospects. Advances in elucidating molecular pathways, such as IL-17 and IFN-I, pave the way for specific treatments. Preclinical studies have revealed the gut microbiome's role in the pathogenesis of MPO-AAV and demonstrate the therapeutic potential of dietary interventions.
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