Th2 dominance in nasal mucosa in patients with Wegener's granulomatosis (Q28347701)

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A J Howie

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A B Drake-Lee

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C O Savage

Clinical and Experimental Immunology

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language of work or name

English

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publication date

August 2001

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published in

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volume

125

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issue

2

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page(s)

332-9

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cites work

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Trimethoprim-sulfamethoxazole (co-trimoxazole) for the prevention of relapses of Wegener's granulomatosis. Dutch Co-Trimoxazole Wegener Study Group

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Wegener's granulomatosis autoantibodies identify a novel diisopropylfluorophosphate-binding protein in the lysosomes of normal human neutrophils

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Autoantibodies developing to myeloperoxidase and proteinase 3 in systemic vasculitis stimulate neutrophil cytotoxicity toward cultured endothelial cells

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T lymphocyte responses to anti-neutrophil cytoplasmic autoantibody (ANCA) antigens are present in patients with ANCA-associated systemic vasculitis and persist during disease remission.

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An interdisciplinary approach to the care of patients with Wegener's granulomatosis: long-term outcome in 155 patients.

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Cytokine profiles in Wegener's granulomatosis: predominance of type 1 (Th1) in the granulomatous inflammation.

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Irregular Cytokine Pattern of CD4+T Lymphocytes in Response toStaphylococcus aureusin Patients with Wegener's Granulomatosis

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Anti-myeloperoxidase antibodies stimulate neutrophils to damage human endothelial cells

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12 December 2020

T cell reactivity to proteinase 3 and myeloperoxidase in patients with Wegener's granulomatosis (WG)

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12 December 2020

T cell responses to myeloperoxidase (MPO) and proteinase 3 (PR3) in patients with systemic vasculitis

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Nasal biopsy in the early diagnosis of Wegener's (pathergic) granulomatosis. Significance of palisading granuloma and leukocytoclastic vasculitis

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Active Wegener's granulomatosis is associated with HLA-DR+ CD4+ T cells exhibiting an unbalanced Th1-type T cell cytokine pattern: reversal with IL-10

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Interleukin-8: A pathogenetic role in antineutrophil cytoplasmic autoantibody-associated glomerulonephritis

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Prominence of cell-mediated immunity effectors in "pauci-immune" glomerulonephritis

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