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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Animals, Autoantibodies, B-Lymphocyte Subsets, Cell Division, Cell Migration Inhibition, Fetal Blood, HIV Antibodies, Humans, Immunoglobulin G, Immunoglobulin M, Infant, Newborn, Kidney Failure, Chronic, Kidney Transplantation, Leukocytes, Lymphocyte Activation, Lymphokines, Mice, Mice, Inbred C57BL, Phosphorylation, Protein Processing, Post-Translational, Receptors, Immunologic, T-Lymphocytes, ZAP-70 Protein-Tyrosine Kinase.
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Do naturally occurring IgM anti-leukocyte autoantibodies inhibit T-cell activation and chemotaxis? Context: Naturally occurring IgM antileukocyte autoantibodies (IgM-ALA) are present from birth and increase during inflammatory processes of diverse etiologies. The clinical observation demonstrating a significant correlation (P < 01) between lack of acute rejections and presence of high levels of IgM-ALA in recipients of kidney allografts prompted us to study if IgM-ALA alters T-cell function and leukocyte chemotaxis. In-vitro functional assays were performed using leucocytes isolated from human peripheral blood. In-vivo studies were performed in C57BL6 mice. Human studies revealed that IgM-ALA consist of several different IgM, each with specificities for a different leukocyte receptor, e.g., CD3, CD4, CCR5, and CXCR4. We show that IgM inhibits T-cell activation, proliferation, and chemotaxis. Data on in vivo murine models of ischemia-reperfusion injury and cardiac transplantation support our hypothesis.
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The innate anti-inflammatory mechanism of IgM-ALA can be exploited by using purified normal IgM to inhibit inflammatory states or by a vaccine approach to increase in vivo production of IgM-ALA (e.g., prior to a transplant). Final Decision: yes