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Toll-like receptors (TLRs) are a family of highly conserved pattern recognition receptors that can recognize both pathogen-associated molecular patterns and danger-associated molecular patterns. These receptors are important in the activation of the innate immune system and play a role in shaping the adaptive immune system. For years, the expression of TLRs in the brain has been proposed to contribute to the immunological protection of the central nervous system. However, emerging studies have provided increasing evidence of non-immune functions of TLRs and suggest that these receptors may participate in more complex processes that extend beyond the regulation of the innate immune response. In this review, we highlight the expression of TLRs in non-immune cells and epitomize TLR non-immune functions. We aim to reveal the novel roles of TLRs that are distinct from their traditional functions in immunity. Negative regulatory approaches used to study TLR signaling pathways are also discussed, providing potential directions for further studies.
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http://dx.doi.org/10.1615/CritRevEukaryotGeneExpr.2018027399 | DOI Listing |
HLA
September 2025
Aix Marseille Univ, CNRS, EFS, ADES, Marseille, France.
Abnormal expression of HLA class Ib, MICA and MICB molecules is associated with the evolution of pathological conditions and clinical settings. Here, we use RNA-sequencing data from two publicly-available projects, from different human organs and tissues and at single-cell level, to present their transcriptional expression throughout the human body, in comparison to that of HLA class Ia, HLA class II, their costimulatory molecules, and the main HLA transcription factors. Our analyses for 21 target genes reveal that median gene expression differs by orders of magnitude and that the classical/non-classical HLA distinction is not absolute for overall expression.
View Article and Find Full Text PDFBiomed Pharmacother
September 2025
Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China. Electronic address:
Immune-mediated necrotizing myopathy (IMNM) is an emerging and severe form of myositis. Most patients experience persistent muscle weakness or recurrent attacks within their lifetime. The previous view suggests that autoimmune and complement activation play a key role in muscle damage, and aggressive immunotherapy may benefit patients.
View Article and Find Full Text PDFJ Med Life
July 2025
Immunology Laboratory, Victor Babes National Institute of Pathology, Bucharest, Romania.
Psoriasis is a chronic inflammatory cutaneous disease with a complex pathogenesis that remains incompletely understood. New data suggest that psoriasis severity may be more accurately assessed by examining inflammation, oxidative stress, and hormones, although further research is needed to substantiate the clinical value of these biomarkers. The multifactorial causes of psoriasis encompass metabolic deregulations, such as lipid alterations that favor inflammation, exacerbate immune cell activity, and worsen the disease symptomatology.
View Article and Find Full Text PDFInt J Mol Sci
August 2025
Department of Dermatology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Galectin-9 (Gal-9, ) is a member of the family of carbohydrate-binding lectins known as galectins. Galectins bind a diverse repertoire of galactose-bearing glycoprotein receptors expressed across multiple cell types. These interactions elicit a broad spectrum of pleiotropic effects important in both normal physiology and disease pathogenesis.
View Article and Find Full Text PDFInt Immunol
August 2025
Department of Immunology, National Institute of Neuroscience, National Center of Neurology and Psychiatry, 4-1-1 Ogawahigashi, Kodaira, Tokyo 187-8502, Japan.
The role of the thyroid hormone receptor beta (TR-β) in the immune system remains poorly understood; although its effect on TGF-βsignaling has been reported in non-immune systems. Here, we report that Thrb is highly expressed in pathogenic CD4+ T cells that infiltrate the central nervous system during experimental autoimmune encephalomyelitis (EAE) and Thrb is exclusively expressed in IL-17-producing CD4+ T cells (Th17 cells) that develop both in vitro or in vivo. Sobetirome, a selective TR-βagonist, promoted pathogenic Th17 differentiation and IL-17 production in the presence of exogenous IL-1β.
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