bims-maitce 2025-01-12 papers

Issue of 2025–01–12
two papers selected by
Andy E. Hogan, Maynooth University

Inflamm Res. 2025 Jan 07. 74(1): 10

MAIT cells modulating the oral lichen planus immune microenvironment: a cellular crosstalk perspective.

Qian Mi, Xiaoli Wu, Yuhe Chen, Wenxia Meng.

Mucosal-associated invariant T (MAIT) cells, a type of T lymphocytes with innate-like characteristics, are crucial in bridging innate and adaptive immunity. When activated, MAIT cells release various inflammatory molecules and swiftly respond to antigens. Notably, numerous studies highlight the significant impact of MAIT cells on tumors and various immune disorders by influencing the immune microenvironment. Oral lichen planus (OLP) is an immune-mediated inflammatory condition mainly involving T lymphocytes. Previous research primarily focused on T cells alone, neglecting the broader immune environment. However, there is a current growing recognition of the complex interactions among multiple immune cells and inflammatory factors in patients with OLP. This immune microenvironment comprises T lymphocytes, fibroblasts, keratinocytes, dendritic cells, macrophages, inflammation-related cytokines, and chemokines, orchestrating intricate interactions that contribute to OLP initiation and persistence. Therefore, this review consolidates current research on the interplay between MAIT cells and other immune cells within the OLP microenvironment. We also delve into potential mechanisms through which MAIT cells regulate inflammation in patients with OLP, aiming to further explore the role of MAIT cells in these patients.

Keywords: Cellular crosstalk; Cytokines; Immune microenvironment; MAIT cells; Oral lichen planus

DOI: https://doi.org/10.1007/s00011-024-01990-6

Alzheimers Dement. 2025 Jan 08. e14480

The MR1/MAIT cell axis enhances dystrophic neurite development in Alzheimer's disease.

Season K Wyatt-Johnson, Samantha Ackley, Jalyn Warren, Raj Priya, Jun Wan, Sheng Liu, Randy R Brutkiewicz.

INTRODUCTION: Plaques are a hallmark feature of Alzheimer's disease (AD). We found that the loss of mucosal-associated invariant T (MAIT) cells and their antigen-presenting molecule MR1 caused a delay in plaque pathology development in AD mouse models. However, it remains unknown how this axis is impacting dystrophic neurites.
METHODS: Brain tissue from 5XFAD mice and those that are MR1 deficient (MR1 KO), were analyzed for dystrophic neurites, amyloid plaques, and synapses via immunofluorescence, RNA sequencing, enzyme-linked immunosorbent assay, and western blot.
RESULTS: In 8-month-old 5XFAD/MR1 KO mice, there was reduced expression of lysosomal-associated membrane protein 1, ubiquitin, and n-terminal amyloid precursor protein in the hippocampus compared to 5XFAD mice (P < 0.05). 5XFAD/MR1 KO mice also had less insoluble amyloid beta 40 (P < 0.001) and higher levels of postsynaptic density protein 95 (P < 0.01) in the hippocampus.
DISCUSSION: Our data contribute additional mechanistic insight into the detrimental role of the MR1/MAIT cell axis in AD pathology development.
HIGHLIGHTS: 5XFAD mice lacking the innate immune MR1/MAIT (mucosal-associated invariant T) cell axis (5XFAD/MR1 KO) have reduced numbers of dystrophic neurite markers in the hippocampus at 8 months of age. Hippocampal tissue transcriptional analyses showed reduced expression of genes encoding classical dystrophic neurite markers in 5XFAD/MR1 KO mice. 5XFAD/MR1 KO mice had less insoluble amyloid beta 40 and increased levels of the post-synaptic marker, postsynaptic density protein 95, in the hippocampus than did MR1+ 5XFAD mice.

Keywords: amyloid plaques; brain pathology; dystrophic neurites; innate immunity; mouse models

DOI: https://doi.org/10.1002/alz.14480