Over the last three decades, autologous hematopoietic stem cell transplantation (AHSCT) has emerged as a significant therapeutic strategy for patients with various refractory autoimmune diseases. Globally, more than 3000 AHSCT procedures have been performed for severe autoimmune diseases. The rationale behind this treatment is abrogation of autoreactivity; renovation of the immune system from the infused hematopoietic stem cells and establishment of a balanced, long-lasting, and self-tolerant immune system. Thymic rebound is a central event in the mechanisms of action of transplantation, promoting the generation of a new repertoire of T cells and reinstating self-tolerance. Here, we critically review the immunological mechanisms of AHSCT in various autoimmune disease settings, with a central focus on thymic rejuvenation. We understand that elucidating the mechanisms of action of the transplant and conducting immunological monitoring studies are crucial for comprehending the risks, benefits, and long-term efficacy of the treatment, thereby promoting functional improvements in patients with autoimmune diseases refractory to conventional treatment.
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http://dx.doi.org/10.1007/978-3-031-77921-3_12 | DOI Listing |
Hematology
December 2025
Department of Medicine, University of Washington, Seattle, WA, United States.
Introduction: Cases of warm autoimmune hemolytic anemia (wAIHA) often present with life-threatening levels of hemoglobin requiring red blood cell (RBC) transfusion support.
Aim: This literature review assessed the occurrence, safety, effectiveness, and hospitalization burden of RBC transfusions in the management of patients with wAIHA.
Methods: Electronic databases (Embase, MEDLINE) were searched from inception to December 2021 along with additional searches conducted up to March 2024.
J Immunol
January 2025
Center for Translational Immunology, Benaroya Research Institute, Seattle, WA, United States.
The CD2-depleting drug alefacept (LFA3-Ig) preserved beta cell function in new-onset type 1 diabetes (T1D) patients. The most promising biomarkers of response were late expansion of exhausted CD8 T cells and rare baseline inflammatory islet-reactive CD4 T cells, neither of which can be used to measure responses to drug in the weeks after treatment. Thus, we investigated whether early changes in T cell immunophenotypes could serve as biomarkers of drug activity.
View Article and Find Full Text PDFJ 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 PDFProc Natl Acad Sci U S A
March 2025
Department of Neurology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9046.
Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by synovial inflammation, pannus formation, and progressive joint destruction. The inflammatory milieu in RA drives endothelial cell activation and upregulation of adhesion molecules, thus facilitating leukocyte infiltration into the synovium. Reelin, a circulating glycoprotein previously implicated in endothelial activation and leukocyte recruitment in diseases such as atherosclerosis and multiple sclerosis, has emerged as a potential upstream regulator of these processes.
View Article and Find Full Text PDFClin Exp Rheumatol
March 2025
Environmental Autoimmunity Group, National Institute of Environmental Health Sciences, National Institutes of Health, Bethesda, MD, and Research Triangle Park, NC, USA.
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