Mucosal-associated invariant T (MAIT) cells are innate T cells that recognize bacteria-infected cells and are thought to play a role in autoimmune diseases. Translocation of duodenal bacteria and viruses to the pancreas through the pancreatic duct has been hypothesized to initiate an innate inflammatory response that could contribute to the development of type 1 diabetes, a process that could involve MAIT cells. In this study, we used immunohistochemistry and quantitative PCR to search for evidence of MAIT cells in the insulitic lesions in the pancreas of human patients recently diagnosed with type 1 diabetes. Only a few scattered MAIT cells were found within the exocrine parenchyma in all pancreatic samples, but no MAIT cells were found in association to the islets. Also, only low gene expression levels of the MAIT T-cell receptor Vα7.2-Jα33 were found in the pancreas of patients with type 1 diabetes, in similar levels as that in nondiabetic organ donors used as control. The absence of MAIT cells shown in insulitic lesions in humans questions the direct cytotoxic role of these cells in β-cell destruction.
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http://dx.doi.org/10.1016/j.ajpath.2018.04.009 | DOI Listing |
Alzheimers Dement
December 2024
Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, USA.
Background: Microglia are dominant immune cells residing in the brain that regulate brain homeostasis and T-cell responses. An important immune function of microglia involves presenting microbial antigens to mucosal-associated invariant T (MAIT) cells; MAIT cells recognize microbial vitamin B-derived metabolites presented by the MHC class I-like molecule, MR1. Our recent findings highlighted a detrimental role for the MR1/MAIT cell axis in Alzheimer's disease (AD) using the 5XFAD mouse model.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, USA.
Background: Plaques are a hallmark feature of Alzheimer's disease (AD). We found the loss of mucosal-associated invariant T (MAIT) cells and its antigen-presenting molecule MR1 caused a delay in plaque pathology development in AD mouse models. However, it remains unknown how this axis is impacting microglial response and dystrophic neurites.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, USA.
Background: We have found that the MHC class I-like MR1 molecule and the innate-like T cells that recognize them (MAIT-mucosal-associated invariant T cells) contribute to the development of pathology in Alzheimer's disease (AD). Moreover, we find elevated levels of MR1 expression and increased numbers of MAIT cells in the brains of 5XFAD mice overtime; these MAIT cells express high surface levels of the T cell activation markers, CD25 and CD69. Here, we are focused on how these two phenomena are connected in AD pathology.
View Article and Find Full Text PDFJ Clin Invest
January 2025
Division of Infection and Immunity, Cardiff University School of Medicine, Cardiff, United Kingdom.
The T cell antigen presentation platform MR1 consists of 6 allomorphs in humans that differ by no more than 5 amino acids. The principal function of this highly conserved molecule involves presenting microbial metabolites to the abundant mucosal-associated invariant T (MAIT) cell subset. Recent developments suggest that the role of MR1 extends to presenting antigens from cancer cells, a function dependent on the K43 residue in the MR1 antigen binding cleft.
View Article and Find Full Text PDFZhongguo Shi Yan Xue Ye Xue Za Zhi
December 2024
Department of Hematology, The Second Hospital of Anhui Medical University, Hefei 230601, Anhui Province, China.
Objective: To explore the changes in number and immune function of mucosal-associated invariant T (MAIT) cells in peripheral blood of patients with newly diagnosed acute myeloid leukemia (AML), and its correlation with the occurrence and development of AML.
Methods: Seventy-five clinical samples of patients with newly diagnosed AML and 48 healthy control samples in our hospital from January 2022 to February 2023 were included. Multiparametric flow cytometry was used to detect the number of MAIT cells, membrane surface markers, effector phenotypes and functional indicators in the samples.
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