TLR8 escapes X chromosome inactivation in human monocytes and CD4


Journal

Biology of sex differences
ISSN: 2042-6410
Titre abrégé: Biol Sex Differ
Pays: England
ID NLM: 101548963

Informations de publication

Date de publication:
18 09 2023
Historique:
received: 19 01 2023
accepted: 04 09 2023
medline: 20 9 2023
pubmed: 19 9 2023
entrez: 18 9 2023
Statut: epublish

Résumé

Human endosomal Toll-like receptors TLR7 and TLR8 recognize self and non-self RNA ligands, and are important mediators of innate immunity and autoimmune pathogenesis. TLR7 and TLR8 are, respectively, encoded by adjacent X-linked genes. We previously established that TLR7 evades X chromosome inactivation (XCI) in female immune cells. Whether TLR8 also evades XCI, however, has not yet been explored. In the current study, we used RNA fluorescence in situ hybridization (RNA FISH) to directly visualize, on a single-cell basis, primary transcripts of TLR7 and TLR8 relative to X chromosome territories in CD14 Using RNA FISH, we show that TLR8, like TLR7, evades XCI in immune cells, and that cells harboring simultaneously TLR7 and TLR8 transcript foci are more frequent in women and KS men than in euploid men, resulting in a sevenfold difference in frequency. This transcriptional bias was again observable when comparing the single X of XY males with the active X of cells from females or KS males. Interestingly, TLR8 protein expression was significantly higher in female mononuclear blood cells, including all monocyte subsets, than in male cells. TLR8, mirroring TLR7, escapes XCI in human monocytes and CD4 Human endosomal Toll-like receptors TLR7 and TLR8, encoded by two adjacent X-linked genes, recognize self and non-self RNA ligands, and are important mediators of innate immunity and autoimmune pathogenesis. We previously reported that TLR7 evades X chromosome inactivation (XCI) in female immune cells, correlating with enhanced functional properties in B cells harboring biallelic expression of this gene. Here, we conducted a comprehensive single-cell resolution analysis of the transcriptional regulation of both TLR7 and TLR8, in CD14

Sections du résumé

BACKGROUND
Human endosomal Toll-like receptors TLR7 and TLR8 recognize self and non-self RNA ligands, and are important mediators of innate immunity and autoimmune pathogenesis. TLR7 and TLR8 are, respectively, encoded by adjacent X-linked genes. We previously established that TLR7 evades X chromosome inactivation (XCI) in female immune cells. Whether TLR8 also evades XCI, however, has not yet been explored.
METHOD
In the current study, we used RNA fluorescence in situ hybridization (RNA FISH) to directly visualize, on a single-cell basis, primary transcripts of TLR7 and TLR8 relative to X chromosome territories in CD14
RESULTS
Using RNA FISH, we show that TLR8, like TLR7, evades XCI in immune cells, and that cells harboring simultaneously TLR7 and TLR8 transcript foci are more frequent in women and KS men than in euploid men, resulting in a sevenfold difference in frequency. This transcriptional bias was again observable when comparing the single X of XY males with the active X of cells from females or KS males. Interestingly, TLR8 protein expression was significantly higher in female mononuclear blood cells, including all monocyte subsets, than in male cells.
CONCLUSIONS
TLR8, mirroring TLR7, escapes XCI in human monocytes and CD4
Human endosomal Toll-like receptors TLR7 and TLR8, encoded by two adjacent X-linked genes, recognize self and non-self RNA ligands, and are important mediators of innate immunity and autoimmune pathogenesis. We previously reported that TLR7 evades X chromosome inactivation (XCI) in female immune cells, correlating with enhanced functional properties in B cells harboring biallelic expression of this gene. Here, we conducted a comprehensive single-cell resolution analysis of the transcriptional regulation of both TLR7 and TLR8, in CD14

Autres résumés

Type: plain-language-summary (eng)
Human endosomal Toll-like receptors TLR7 and TLR8, encoded by two adjacent X-linked genes, recognize self and non-self RNA ligands, and are important mediators of innate immunity and autoimmune pathogenesis. We previously reported that TLR7 evades X chromosome inactivation (XCI) in female immune cells, correlating with enhanced functional properties in B cells harboring biallelic expression of this gene. Here, we conducted a comprehensive single-cell resolution analysis of the transcriptional regulation of both TLR7 and TLR8, in CD14

Identifiants

pubmed: 37723501
doi: 10.1186/s13293-023-00544-5
pii: 10.1186/s13293-023-00544-5
pmc: PMC10506212
doi:

Substances chimiques

Toll-Like Receptor 8 0
Toll-Like Receptor 7 0
TLR8 protein, human 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

60

Informations de copyright

© 2023. Society for Women's Health Research and BioMed Central Ltd.

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Auteurs

Ali Youness (A)

Institut Toulousain des Maladies Infectieuses et Inflammatoires (INFINITY), UMR 1291 INSERM, CNRS, Hôpital Purpan, Université de Toulouse, 31024, Toulouse, France.

Claire Cenac (C)

Institut Toulousain des Maladies Infectieuses et Inflammatoires (INFINITY), UMR 1291 INSERM, CNRS, Hôpital Purpan, Université de Toulouse, 31024, Toulouse, France.

Berenice Faz-López (B)

Institut Toulousain des Maladies Infectieuses et Inflammatoires (INFINITY), UMR 1291 INSERM, CNRS, Hôpital Purpan, Université de Toulouse, 31024, Toulouse, France.

Solange Grunenwald (S)

Service d'Endocrinologie, Maladies Métaboliques et Nutrition, Hôpital Larrey, Centre Hospitalier Universitaire (CHU) de Toulouse, 31059, Toulouse, France.

Franck J Barrat (FJ)

Hospital for Special Surgery, HSS Research Institute and David Z. Rosensweig Genomics Research Center, New York, NY, 10021, USA.
Department of Microbiology and Immunology, Weill Cornell Medical College of Cornell University, New York, NY, 10021, USA.

Julie Chaumeil (J)

INSERM, CNRS, Université Paris Cité, Institut Cochin, 75014, Paris, France.

José Enrique Mejía (JE)

Institut Toulousain des Maladies Infectieuses et Inflammatoires (INFINITY), UMR 1291 INSERM, CNRS, Hôpital Purpan, Université de Toulouse, 31024, Toulouse, France. jose-enrique.mejia@inserm.fr.

Jean-Charles Guéry (JC)

Institut Toulousain des Maladies Infectieuses et Inflammatoires (INFINITY), UMR 1291 INSERM, CNRS, Hôpital Purpan, Université de Toulouse, 31024, Toulouse, France. jean-charles.guery@inserm.fr.

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