Improving lymphatic flow in SLE mice induces fibroblastic reticular cell survival via lymphotoxin beta receptor signaling.

نویسندگان

چکیده

Abstract Systemic lupus erythematosus (SLE) patients are photosensitive, where ultraviolet radiation (UVR) exposure can induce skin inflammation and also trigger systemic disease flares. The link between photosensitive autoimmunity is not well understood. Skin communicates with the immune system via lymphatic vessels that carry lymph into conduit of nodes (LNs), which ensheathed by fibroblastic reticular cells (FRCs). FRCs play critical roles in limiting T B cell responses. Dendritic (DCs) interact both fluid modulate FRC survival numbers a DC-lymphotoxin beta receptor (LTβR)-FRC axis. We have recently shown dysfunctional flow human SLE mouse models exposed to UVR improving manual drainage (MLD) reduces photosensitivity LN plasmablast responses, while increasing numbers. In this study, we aim delineate mechanism MLD induces alterations, hypothesizing it DC-LTβR-FRC Currently, found increases mice. However, treatment antagonist LTbR-Ig reverses survival, suggesting LTbR signaling. Ongoing experiments targeting importance DCs DC-derived LTβ modulating MLD-induced changes FRCs. novelty study showing from influence stromal populations SLE. These findings will improve our understanding relationship autoimmunity.

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ژورنال

عنوان ژورنال: Journal of Immunology

سال: 2023

ISSN: ['1550-6606', '0022-1767']

DOI: https://doi.org/10.4049/jimmunol.210.supp.176.12