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Exploring MHC Class II I-Ab Blockade as a Potential Treatment for Sjögren’s Disease in the Mouse Model

ABSTRACT: Exploring MHC Class II I-Ab Blockade as a Potential Treatment for Sjögren’s Disease in the Mouse Model

PROVIDER: PRJNA1228800 | ENA |

REPOSITORIES: ENA

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Exploring MHC Class II I-Ab Blockade as a Potential Treatment for Sjögren’s Disease in the Mouse Model

Project description:Sjögren’s disease (SjD) is a chronic autoimmune disorder predominantly affecting females, characterized by exocrine gland dysfunction. This study investigates the therapeutic potential of 2-chloro-1-(4-hydroxy-phenyl)-ethanone (CHPE) and metformin in the C57BL/6.NOD-Aec1Aec2 mouse model, which closely mirrors human SjD. Molecular docking identified CHPE and metformin as high-affinity binders to the MHC class II I-Ab antigen-binding groove, suggesting their ability to inhibit antigen presentation and modulate immune responses. In-vitro assays confirmed their effectiveness in reducing T cell activation. In-vivo studies demonstrated that both preventative and therapeutic regimens of CHPE and metformin significantly reduced lymphocytic infiltration in the lacrimal glands, with metformin showing a more pronounced effect in females. Salivary gland infiltration was less responsive, though some reduction in focal scores was observed in male mice treated preventatively with CHPE. Both drugs altered the composition of lymphocytic infiltrates, particularly by reducing B cell populations, with notable sex-specific differences in response to treatment. CHPE and metformin also reduced anti-nuclear antibody levels, with CHPE showing stronger effects in females. Additionally, both drugs improved saliva and tear secretion, with metformin being more effective in the preventative regimen, especially in females. T cell receptor transductant assays revealed that CHPE and metformin exert their therapeutic effects through antigen-specific pathways, inhibiting T cell responses to SjD-associated autoantigens. Overall, this study provides compelling evidence that CHPE and metformin can modulate immune responses and improve gland function, with effectiveness varying by sex and age. These findings support the potential of these compounds as personalized treatments for SjD tailored to individual patient characteristics.

2025-09-03 | GSE290595 | GEO

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Acrocephalus schoenobaenus MHC class I

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Exploring MHC class II I-Ab blockade as a potential treatment for Sjogren’s disease in the mouse model

Project description: Not available

| S-EPMC12377902 | biostudies-literature

Analysis of MHC class II peptides

Project description:Peptides eluted from MHC class II (I-Ak) to which HEL protein was pulsed.

2026-03-09 | PXD075403 | JPOST Repository

MHC class I and MHC class II reporter mice enable analysis of immune oligodendroglia in mouse models of multiple sclerosis

Project description:Oligodendrocytes and their progenitors upregulate MHC pathways in response to inflammation, but the frequency of this phenotypic change is unknown and the features of these immune oligodendroglia are poorly defined. We generated MHC class I and II transgenic reporter mice to define their dynamics in response to inflammatory demyelination, providing a means to monitor MHC activation in diverse cell types in living mice and define their roles in aging, injury and disease.

2022-09-23 | GSE213739 | GEO

MHC Class I on Target Cells Regulates CD4+ T cell-mediated Immunity

Project description:The central tenet of T cell immune surveillance is that MHC class I and class II molecules present antigens to CD8+ and CD4+ T cells, respectively. Here, we uncover a surprising and previously unrecognized role for MHC class I in modulating CD4+ T cell-mediated immunity. Using multiple in vivo models of allogeneic graft-versus-host disease (GVHD) and tumor immunity, we demonstrate that the absence of MHC class I on target cells significantly increases their susceptibility to CD4+ T cell cytotoxicity. Transcriptomic and functional studies indicate this heightened sensitivity to enhanced ferroptosis of the target cells without affecting the degree of CD4+ T cell activation or inflammatory responses. The experimental results are corroborated utilizing multiple large human transcriptomic and sequencing datasets that suggest a role for CD4+ T cells in enhancing immune checkpoint blocker-mediated responses in patients with melanoma and mismatch repair-deficient (MMRd) colon cancers that have downregulated MHC class I. These findings revise and expand the known role of MHC class I in CD8+ T cell and NK cell immunity and demonstrate a previously unrecognized role in CD4+ T cell-mediated cancer and alloimmunity.

2026-02-02 | GSE316959 | GEO

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