0000000000194722

AUTHOR

C. Preusse

showing 3 related works from this author

Th2-M2 immunity in lesions of muscular sarcoidosis and macrophagic myofasciitis

2015

Objective To analyse the paradox of a lack of giant cell formation and fibrosis in chronic lesions of macrophagic myofasciitis (MMF) in comparison with muscular sarcoidosis (MuS). Methods Inflammatory lesions and contiguous muscle regions from biopsy samples of 10 patients with MuS and 10 patients with MMF were cut out by laser microdissection. Mediators of the T helper cell (Th)1 inducing classical macrophage activation (e.g. STAT1, IFNγ and CXCR3), and Th2 inducing alternative activation of macrophages (e.g. CD206/MRC1, STAT6, SOCS1), molecules involved in development of fibrosis (e.g. TGFβ) and giant cells (e.g. TYROBP), were assessed by immunohistochemistry and real-time polymerase chai…

Pathologymedicine.medical_specialtyHistologyMacrophagic myofasciitisT helper cellBiologyCXCR3medicine.diseasePathology and Forensic Medicinemedicine.anatomical_structureNeurologyFibrosisGiant cellPhysiology (medical)GranulomamedicineMacrophageNeurology (clinical)Laser capture microdissectionNeuropathology and Applied Neurobiology
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P.21.2 New insights into eosinophilic fasciitis

2013

Eosinophilic fasciitis (EF), first described by Shulman in 1974, is a rare disease characterized by fibrosis and inflammatory infiltration of the muscle fascia as well as scleroderma-like skin indurations and blood eosinophilia. In contrast to other inflammatory myopathies, patients generally show less muscle weakness and myalgia, and a frequent increase in body weight. Thus, we hypothesize a unique immune mechanism underlying Shulman syndrome. The immunohistochemical expression pattern of leucocytes and a comprehensive panel of cytokine and chemokine expression on RNA level of muscle specimen from EF patients were compared to healthy control muscle. In patients with biopsy-proven EF the im…

ChemokinePathologymedicine.medical_specialtybiologymedicine.medical_treatmentT helper cellmedicine.diseaseEosinophilic fasciitisImmune systemmedicine.anatomical_structureCytokineNeurologyPediatrics Perinatology and Child HealthMHC class IImmunologybiology.proteinmedicineMacrophageNeurology (clinical)Genetics (clinical)CD8Neuromuscular Disorders
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P.20.3 Targeting fibrosis and inflammation in Duchenne Muscular Dystrophy

2013

Duchenne Muscular Dystrophy is the most frequent genetic muscle disease worldwide affecting ∼1:5000 male births. It is caused by a defective DMD gene, which leads to reduced and defective dystrophin protein expression. The constant breakdown of fibres leads to focal necrosis, myophagocytosis and a considerable influx of inflammatory cells into the muscle tissue, which is followed by increasing endomysial fibrosis. Both, inflammation and fibrosis as well as a putative relation are not yet understood immunologically. Fibrosis directly correlates with adverse outcome and early loss of ambulation. We have studied how inflammation is linked to fibrosis in DMD, with an emphasis on the communicati…

Muscle biopsymedicine.diagnostic_testbiologyDuchenne muscular dystrophyInflammationDiseasemedicine.diseasePhenotypeImmune systemNeurologyFibrosisPediatrics Perinatology and Child HealthImmunologymedicinebiology.proteinNeurology (clinical)medicine.symptomDystrophinGenetics (clinical)Neuromuscular Disorders
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