Interactions of the humoral pattern recognition molecule PTX3 with the complement system

Immunobiology ◽  
2012 ◽  
Vol 217 (11) ◽  
pp. 1122-1128 ◽  
Author(s):  
Andrea Doni ◽  
Cecilia Garlanda ◽  
Barbara Bottazzi ◽  
Seppo Meri ◽  
Peter Garred ◽  
...  
2020 ◽  
Vol 204 (6) ◽  
pp. 1598-1606
Author(s):  
Nikolaj Kirketerp-Møller ◽  
Rafael Bayarri-Olmos ◽  
Karen Angeliki Krogfelt ◽  
Peter Garred

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 223.3-223
Author(s):  
E. Lovšin ◽  
J. Kovac ◽  
T. Tesovnik ◽  
N. Toplak ◽  
D. Perko ◽  
...  

Background:Periodic fever, aphthous stomatitis, pharyngitis and adenitis (PFAPA) syndrome is the most common autoinflammatory disease in children, often grouped together with hereditary periodic fever syndromes, although its cause and hereditary nature remain unexplained.Objectives:We investigated whether a differential DNA methylation was present in DNA from peripheral blood mononuclear cells (PBMC) in patients with PFAPA versus a group of healthy young individuals.Methods:A whole epigenome analysis (MeDIP and MBD) was performed using pooled DNA libraries enriched for methylated genomic regions. Of identified candidate genes, two with most significantly different methylation leves were further evaluated with methylation specific restriction enzymes coupled with qPCR (MSRE-qPCR).Results:The analysis showed thatPIK3AP1andSPON2intronic gene regions are differentially methylated in patients with PFAPA. MSRE-qPCR proved as a quick, reliable and cost-effective method to confirm results from MeDIP and MBD.Conclusion:Our findings indicate that B cell adapter protein (BCAP) as PI3K binding inhibitor of inflammation and spondin-2 (SPON2) as a pattern recognition molecule and integrin ligand could play a role in etiology of PFAPA. Their role and impact of changed DNA methylation in PFAPA etiology and autoinflammation need further investigation.References:[1]Wekell P. Periodic fever, aphthous stomatitis, pharyngitis, and cervical adenitis syndrome – PFAPA syndrome. Press Medicale [Internet]. 2019;48(1):e77–87. Available from:https://doi.org/10.1016/j.lpm.2018.08.016[2]K. Theodoropoulou, F. Vanoni, and M. Hofer, “Periodic Fever, Aphthous Stomatitis, Pharyngitis, and Cervical Adenitis (PFAPA) Syndrome: a Review of the Pathogenesis,”Curr. Rheumatol. Rep., vol. 18:18, 2016.[3]Carpentier SJ, Ni M, Duggan JM, James RG, Cookson BT, Hamerman JA. The signaling adaptor BCAP inhibits NLRP3 and NLRC4 inflammasome activation in macrophages through interactions with Flightless-1. Sci Signal. 2019;12(581).[4]He YW, Li H, Zhang J, Hsu CL, Lin E, Zhang N, et al. The extracellular matrix protein mindin is a pattern-recognition molecule for microbial pathogens. Nat Immunol. 2004;5(1):88–97.Disclosure of Interests:None declared


2015 ◽  
Vol 42 (7) ◽  
pp. 1252-1258 ◽  
Author(s):  
Christine Petri ◽  
Steffen Thiel ◽  
Jens Christian Jensenius ◽  
Troels Herlin

Objective.The complement system plays a crucial role in the pathogenesis of inflammatory processes. The lectin pathway of the complement system is activated through the recognition of pathogens by soluble pattern recognition molecules (PRM), i.e., mannan-binding lectin (MBL), collectin-LK, and the ficolins. PRM are reportedly correlated to disease activity in rheumatoid arthritis (RA). The aim was to evaluate the pathogenic role of PRM in juvenile idiopathic arthritis (JIA).Methods.We measured MBL, M-ficolin, H-ficolin, MBL-associated serine proteases (MASP) 1, MASP-2, MASP-3, and 2 alternative splice products, MBL-associated protein (MAp) 44 and MAp19, in plasma and synovial fluid (SF) of children with persistent oligoarticular (n = 109 in plasma, n = 38 in SF) and systemic JIA (n = 19 in plasma, n = 11 in SF). The concentrations of the proteins were measured by in-house time-resolved immunofluorometric assays.Results.We observed significantly higher levels of M-ficolin, MASP-1, MASP-2, and MASP-3 in plasma and SF from patients with systemic JIA compared with persistent oligoarticular JIA (p < 0.001). In paired samples of plasma and SF from 47 patients with oligoarticular and systemic JIA, we observed higher concentrations in plasma for both subtypes for 7 of the measured proteins while the reverse relationship was observed for MASP-3. M-ficolin and MASP-2 correlated to erythrocyte sedimentation rate, C-reactive protein, white blood cell count, and platelet count (p < 0.001). M-ficolin was in addition related to the number of active joints and inversely related to hemoglobin levels.Conclusion.Our results point to plasma M-ficolin and MASP-2 as inflammatory markers in JIA. The levels of all proteins are higher in plasma than in SF, except for MASP-3, indicating that MASP-3 may be produced locally in joints.


2012 ◽  
Vol 287 (11) ◽  
pp. 8071-8081 ◽  
Author(s):  
Rikke M. Zacho ◽  
Lisbeth Jensen ◽  
Randi Terp ◽  
Jens C. Jensenius ◽  
Steffen Thiel

2009 ◽  
Vol 28 (3) ◽  
pp. 286-297 ◽  
Author(s):  
Yili Li ◽  
Chunzhang Cao ◽  
Wei Jia ◽  
Lily Yu ◽  
Min Mo ◽  
...  

2016 ◽  
Vol 38 ◽  
pp. 39-44 ◽  
Author(s):  
Cecilia Garlanda ◽  
Sebastien Jaillon ◽  
Andrea Doni ◽  
Barbara Bottazzi ◽  
Alberto Mantovani

2011 ◽  
Vol 186 (9) ◽  
pp. 5425-5434 ◽  
Author(s):  
Federica Moalli ◽  
Moira Paroni ◽  
Tania Véliz Rodriguez ◽  
Federica Riva ◽  
Nadia Polentarutti ◽  
...  

2010 ◽  
Vol 28 (1) ◽  
pp. 131-155 ◽  
Author(s):  
Claudia Kemper ◽  
John P. Atkinson ◽  
Dennis E. Hourcade

2004 ◽  
Vol 279 (46) ◽  
pp. 47513-47519 ◽  
Author(s):  
Anders Krarup ◽  
Steffen Thiel ◽  
Annette Hansen ◽  
Teizo Fujita ◽  
Jens C. Jensenius

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