In the present study, we report that Cy-sensitive, MRAG-adherent spleen mononuclear (SpM) inductor-phase T suppressor (Ts) cells obtained from rats pretreated with low doses of a purified fraction (FI) of rat male accessory gland antigens (RAG) are mainly OX19+ and W3/25+. Furthermore, thymocytes from rats pretreated with FI of RAG restore the suppression of the autoimmune response to RAG autoantigens in irradiated recipients of SpM inductor-phase Ts cells. In contrast, thymocytes from rats pretreated with rat heart saline extract (unrelated antigen) did not recuperate the suppression of the autoimmune response detected by macrophage migration inhibitory factor (MIF) and delayed-type hypersensitivity. The suppressor thymocytes did not directly exert their inhibitory effect because they were not effective to suppress the autoimmune response to RAG autoantigens when irradiated recipients did not receive SpM inductor-phase Ts cells. The effect of these thymocytes was found in PNA--but not in PNA+ thymic cell population. The perithymic injection of Toxoplasma gondii did block their suppressor activity. The present report clearly shows an active participation of thymus in the efferent phase of the suppressor circuit that controls the autoimmune response to MRAG. The implications of these findings are discussed.
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http://dx.doi.org/10.3109/08916939109007644 | DOI Listing |
Br J Dermatol
January 2025
Inflammatory Immune-Mediated Chronic Skin Diseases Laboratory (GC26), Maimonides Biomedical Research Institute of Cordoba (IMIBIC)/University of Cordoba/Reina Sofia University Hospital, Menendez Pidal Ave, 14004, Córdoba, Spain.
Introduction: Non-segmental vitiligo (NSV) is an autoimmune condition characterized by melanocyte loss. While skin-specific mechanisms are well-studied, systemic immune dysregulation contributing to NSV pathogenesis remains unclear.
Objective: This study employs a multi-omic single-cell approach to investigate circulating immune cells in NSV, integrating transcriptional and chromatin accessibility data.
Immunol Rev
March 2025
Department of Immunology, Moffitt Cancer Center, Tampa, Florida, USA.
The immune checkpoint receptor lymphocyte activation gene-3 (LAG3) inhibits T-cell activation and was recently validated as a target for cancer immunotherapy. Despite its emergence as a therapeutic target, a lack of molecular-level insight has obscured our understanding of the LAG3 immunosuppression mechanism. This review highlights a series of breakthroughs that have illuminated fundamental aspects of LAG3 molecular biology.
View Article and Find Full Text PDFAdv Sci (Weinh)
January 2025
Department of Gastroenterology, Changhai Hospital, Shanghai, 200433, China.
Autoimmune pancreatitis (AIP) is identified as a severe chronic immune-related disorder in pancreas, including two subtypes. In this study, pancreatic lesions in patients diagnosed as either type 1 AIP or type 2 AIP are examined, and these patients' peripheral blood at single-cell level. Furthermore, flow cytometry, immunofluorescence, and functional assays are performed to verify the identified cell subtypes.
View Article and Find Full Text PDFCurr Opin Psychiatry
March 2025
Department of Neurology and Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, Minnesota, USA.
Purpose Of Review: The aim of this review is to summarize clinical, radiological and laboratory findings in autoimmune dementia, to help clinicians in promptly identify this elusive condition.
Recent Findings: The rapid advances in the field of autoimmune neurology have led to the discovery of novel antibodies and associated disorders, which are more frequent than previously hypothesized. The correct and prompt identification of cognitive decline of autoimmune origin is vital to ensure early treatment and better outcomes.
Gastroenterol Hepatol (N Y)
November 2024
Lily and Terry Horner Chair in Autoimmune Liver Disease Research Professor of Medicine, Division of Gastroenterology and Hepatology University of Toronto The Autoimmune and Rare Liver Disease Programme Toronto General Hospital Toronto, Ontario, Canada.
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