Retinoic acid modulates nod-like receptor-mediated responses in human macrophages

A tétel rövid nézete
dc.contributor.advisorBenkő, Szilvia
dc.contributor.authorAlatshan, Ahmad
dc.contributor.authorvariantAlatshan, Ahmad
dc.contributor.departmentMolekuláris sejt- és immunbiológia doktori iskolahu
dc.contributor.submitterdepÁltalános Orvostudományi Kar
dc.date.accessioned2026-03-10T18:43:42Z
dc.date.available2026-03-10T18:43:42Z
dc.date.defended2026-03-26
dc.date.issued2026
dc.description.abstractMacrophages (MΦs) are crucial innate immune effector cells involved in a wide range of biological processes, including host immune defense and tissue homeostasis. MΦs surveil the local environment by utilizing several groups of sensing receptors, such as cytokine receptors, nuclear hormone receptors and pattern recognition receptors (PRRs). Activation of these receptors in turn determine the MΦs fate and the outcome of immune responses. Among the PRRs, NOD-like receptors (NLRs) are a group of conserved cytosolic proteins, that recognize microbial and host danger signals and initiate innate immune responses. Besides, NLRs are implicated in regulation of gene expression, signaling pathways, reproduction; and some NLRs trigger inflammasome formation. However, dysfunction of NLRs is associated with various inflammatory diseases and autoimmune diseases, in line, targeting these receptors or modulate its functions may provide promising option for novel therapeutics targets. Since MΦs functions can be also regulated by nuclear receptors that sense endogenous or exogenous lipid compounds, all-trans retinoic acid (ATRA) arises as tissue-derived signal and an endogenous ligand for nuclear receptors that may modulate the MΦs activity. ATRA is the most metabolically active form of vitamin A, and has been approved by Food and Drug Administration (FDA) for treating acute promyelocytic leukemia. ATRA is an essential component in certain tissue microenvironments where it is necessary for the proper functions of immune cells. However, there is less known about the role of ATRA in regulating specific NLR-mediated response in MΦs. We hypothesized that ATRA modulates selected, NLR-mediated functions in human MΦs. In our study, we targeted NLRs characterized with different functions: (1) inflammasome forming NLR (NLRP3); and (2) regulatory NLRs of inflammatory signaling (NOD1 and NOD2). These proteins belong to those few NLRs that have well-characterized agonists and antagonists for molecular manipulation. Our data reveals that ATRA is capable to modulate the NLR-mediated responses via several potential mechanisms. Our findings raise the importance of ATRA in regulating NLR-mediated pathways and the outcome of related inflammatory responses, and highlights that targeting nuclear receptors is a promising strategy for the treatment of various infectious and chronic inflammatory conditions that are associated with NLR dysfunction.
dc.format.extent82
dc.identifier.urihttps://hdl.handle.net/2437/405481
dc.language.isoen
dc.subjectRetinoic acid
dc.subjectNod-like receptors
dc.subjectInflammasome
dc.subjectCytokine
dc.subject.disciplineElméleti orvostudományokhu
dc.subject.sciencefieldOrvostudományokhu
dc.titleRetinoic acid modulates nod-like receptor-mediated responses in human macrophages
dc.title.translatedA retinsav modulálja a Nod-like receptorok által közvetített válaszokat humán makrofágokon
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