Layilin Regulates Treg Motility and Suppressive Capacity in Skin
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Abstract
Regulatory T cells (Tregs) are essential for maintaining immune tolerance in both lymphoid and non-lymphoid tissues. We discovered that layilin, a C-type lectin receptor, is predominantly expressed on Tregs in skin. Layilin was highly expressed on a subset of clonally expanded ‘effector’ Tregs in both healthy and psoriatic skin. Layilin expressing Tregs exhibited a transcriptional profile indicative of enhanced adhesion. Deletion of layilin in Tregs in vivo resulted in significantly attenuated skin inflammation. Mechanistically, layilin enhanced Treg adhesion via modulation of LFA-1, resulting in distinct cytoskeletal alterations consistent with enhanced focal adhesion and lamellipodia formation. Taken together, we define layilin as a critical regulator of Treg suppressive capacity through modulating motility and adhesion in a non-lymphoid tissue.
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However, more research is necessary to understand the role of layilin on non-immune cells, such as gastrointestinal epithelial cells (9, 46) to help build confidence around this therapeutic hypothesis
Is there a complete layilin knockout or other tissue-specific conditional knockouts that provide insight into layilin’s role in other cells/tissues?
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Conversely, in pathological situations such as tumors and chronic inflammation, the motility of Tregs may play a larger role in their functionality, allowing them to navigate to various tissue microanatomic niches to attenuate specific cell types and inflammatory mediators.
Congratulations on the elegant study! I'm curious if there are layilin mutations associated with with chronic inflammation or highly metastatic carcinomas?
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