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- Thomas, HS, et al.
(författare)
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- 2019
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swepub:Mat__t
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- Adami, C., et al.
(författare)
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The XXL Survey: XX. The 365 cluster catalogue
- 2018
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Ingår i: Astronomy and Astrophysics. - : EDP Sciences. - 0004-6361 .- 1432-0746. ; 620
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Tidskriftsartikel (refereegranskat)abstract
- Context. In the currently debated context of using clusters of galaxies as cosmological probes, the need for well-defined cluster samples is critical. Aims. The XXL Survey has been specifically designed to provide a well characterised sample of some 500 X-ray detected clusters suitable for cosmological studies. The main goal of present article is to make public and describe the properties of the cluster catalogue in its present state, as well as of associated catalogues of more specific objects such as super-clusters and fossil groups. Methods. Following from the publication of the hundred brightest XXL clusters, we now release a sample containing 365 clusters in total, down to a flux of a few 10-15 erg s-1 cm-2 in the [0.5-2] keV band and in a 1′ aperture. This release contains the complete subset of clusters for which the selection function is well determined plus all X-ray clusters which are, to date, spectroscopically confirmed. In this paper, we give the details of the follow-up observations and explain the procedure adopted to validate the cluster spectroscopic redshifts. Considering the whole XXL cluster sample, we have provided two types of selection, both complete in a particular sense: one based on flux-morphology criteria, and an alternative based on the [0.5-2] keV flux within 1 arcmin of the cluster centre. We have also provided X-ray temperature measurements for 80% of the clusters having a flux larger than 9 × 10-15 erg s-1 cm-2. Results. Our cluster sample extends from z ∼ 0 to z ∼ 1.2, with one cluster at z ∼ 2. Clusters were identified through a mean number of six spectroscopically confirmed cluster members. The largest number of confirmed spectroscopic members in a cluster is 41. Our updated luminosity function and luminosity-temperature relation are compatible with our previous determinations based on the 100 brightest clusters, but show smaller uncertainties. We also present an enlarged list of super-clusters and a sample of 18 possible fossil groups. Conclusions. This intermediate publication is the last before the final release of the complete XXL cluster catalogue when the ongoing C2 cluster spectroscopic follow-up is complete. It provides a unique inventory of medium-mass clusters over a 50 deg2 area out to z ∼ 1.
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- Hsieh, W. C., et al.
(författare)
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PTPN2 links colonic and joint inflammation in experimental autoimmune arthritis
- 2020
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Ingår i: Jci Insight. - : American Society for Clinical Investigation. - 2379-3708. ; 5:20
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Tidskriftsartikel (refereegranskat)abstract
- Loss-of-function variants of protein tyrosine phosphatase non-receptor type 2 (PTPN2) enhance risk of inflammatory bowel disease and rheumatoid arthritis; however, whether the association between PTPN2 and autoimmune arthritis depends on gut inflammation is unknown. Here we demonstrate that induction of subclinical intestinal inflammation exacerbates development of autoimmune arthritis in SKG mice. Ptpn2-haploinsufficient SKG mice - modeling human carriers of disease-associated variants of PTPN2 - displayed enhanced colitis-induced arthritis and joint accumulation of Tregs expressing RAR-related orphan receptor gamma T (ROR-gamma t) - a gut-enriched Treg subset that can undergo conversion into FoxP3 IL-17(+) arthritogenic exTregs. SKG colonic Tregs underwent higher conversion into arthritogenic exTregs when compared with peripheral Tregs, which was exacerbated by haploinsufficiency of Ptpn2. Ptpn2 haploinsufficiency led to selective joint accumulation of ROR gamma t-expressing Tregs expressing the colonic marker G protein-coupled receptor 15 (GPR15) in arthritic mice and selectively enhanced conversion of GPR15(+). Tregs into exTregs in vitro and in vivo. Inducible Treg-specific haploinsufficiency of Ptpn2 enhanced colitis-induced SKG arthritis and led to specific joint accumulation of GPR15(+). exTregs. Our data validate the SKG model for studies at the interface between intestinal and joint inflammation and suggest that arthritogenic variants of PTPN2 amplify the link between gut inflammation and arthritis through conversion of colonic Tregs into exTregs.
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- McBride, D. A., et al.
(författare)
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Immunomodulatory Microparticles Epigenetically Modulate T Cells and Systemically Ameliorate Autoimmune Arthritis
- 2023
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Ingår i: Advanced Science. - : Wiley. - 2198-3844. ; 10:11
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Tidskriftsartikel (refereegranskat)abstract
- Disease modifying antirheumatic drugs (DMARDs) have improved the prognosis of autoimmune inflammatory arthritides but a large fraction of patients display partial or nonresponsiveness to front-line DMARDs. Here, an immunoregulatory approach based on sustained joint-localized release of all-trans retinoic acid (ATRA), which modulates local immune activation and enhances disease-protective T cells and leads to systemic disease control is reported. ATRA imprints a unique chromatin landscape in T cells, which is associated with an enhancement in the differentiation of naive T cells into anti-inflammatory regulatory T cells (T-reg) and suppression of T-reg destabilization. Sustained release poly-(lactic-co-glycolic) acid (PLGA)-based biodegradable microparticles encapsulating ATRA (PLGA-ATRA MP) are retained in arthritic mouse joints after intra-articular (IA) injection. IA PLGA-ATRA MP enhance migratory T-reg which in turn reduce inflammation and modify disease in injected and uninjected joints, a phenotype that is also reproduced by IA injection of T-reg. PLGA-ATRA MP reduce proteoglycan loss and bone erosions in the SKG and collagen-induced arthritis mouse models of autoimmune arthritis. Strikingly, systemic disease modulation by PLGA-ATRA MP is not associated with generalized immune suppression. PLGA-ATRA MP have the potential to be developed as a disease modifying agent for autoimmune arthritis.
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- Orrú, Valeria, et al.
(författare)
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A loss-of-function variant of PTPN22 is associated with reduced risk of systemic lupus erythematosus
- 2009
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Ingår i: Human Molecular Genetics. - : Oxford University Press (OUP). - 0964-6906 .- 1460-2083. ; 18:3, s. 569-579
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Tidskriftsartikel (refereegranskat)abstract
- A gain-of-function R620W polymorphism in the PTPN22 gene, encoding the lymphoid tyrosine phosphatase LYP, has recently emerged as an important risk factor for human autoimmunity. Here we report that another missense substitution (R263Q) within the catalytic domain of LYP leads to reduced phosphatase activity. High-resolution structural analysis revealed the molecular basis for this loss of function. Furthermore, the Q263 variant conferred protection against human systemic lupus erythematosus, reinforcing the proposal that inhibition of LYP activity could be beneficial in human autoimmunity.
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