Elevated interleukin-4 and interleukin-13 production by T cell lines from patients with Churg-Strauss syndrome

Kiene, Miriam; Csernok, Elena; Müller, Antje; Metzler, Claudia; Trabandt, Andreas; Gross, Wolfgang L.

doi:10.1002/1529-0131(200102)44:2<469::aid-anr66>3.0.co;2-0

Cited by 138 publications

(58 citation statements)

References 20 publications

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“…Churg-Strauss syndrome (CSS), also known as allergic granulomatosis and angiitis, is another asthma-related disorder characterized by systemic small vessel vasculitis. Indeed, analysis of the cytokine profile of T cell lines from patients with CSS has shown both type-1 cytokine and type-2 cytokine responses (Kiene et al 2001). Of note, clinical signs of autoimmunity such as vasculitis have been observed in some patients with AIA (Szczeklik et al 1995.…”

Section: Discussionmentioning

confidence: 99%

Functional promoter polymorphism in the TBX21 gene associated with aspirin-induced asthma

et al. 2005

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Asthma is a phenotypically heterogeneous disorder with many etiologic factors and clinical characteristics. T-bet, a Th1-specific transcription factor of T-box family, has been found to control interferon-gamma (IFN-gamma) expression in T cells. Mice lacking the T-bet gene (tbx21) demonstrate multiple physiological and inflammatory features reminiscent of human asthma. In order to examine whether polymorphisms in the candidate gene, TBX21, located on chromosome 17q21.32, are related to the risk of human asthma phenotypes, we have searched for genetic variations in the human TBX21 gene and identified 24 single nucleotide polymorphisms (SNPs), including five novel SNPs, by direct sequencing in Japanese subjects. Among asthma phenotypes, a promoter -1993T-->C SNP, which is in linkage disequilibrium with a synonymous coding 390A-->G SNP in exon 1, is significantly associated with a risk of aspirin-induced asthma (AIA; P = 0.004, P(c) = 0.016). This association has also been confirmed in additional independent samples of asthma with nasal polyposis (P = 0.008), regardless of aspirin hypersensitivity. Furthermore, our data indicate that the -1993T-->C substitution increases the affinity of a particular nuclear protein to the binding site of TBX21 covering the -1993 position, resulting in increased transcriptional activity of the TBX21 gene. Thus, in addition to the antigen-driven excess Th2 response, increased T-bet (and subsequent IFN-gamma) production in human airways of individuals with the -1993T-->C polymorphism could contribute to the development of certain asthma-related phenotypes, such as AIA.

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Section: Discussionmentioning

confidence: 99%

Functional promoter polymorphism in the TBX21 gene associated with aspirin-induced asthma

et al. 2005

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“…12,13 Interleukin (IL)-5 production is increased in patients with EGPA and is involved in the maturation and survival of eosinophils. 14,15 Other Th2 cytokines, such as IL-4 and IL-13, have also been found to be increased in EGPA, 15,16 leading to the hypothesis that this may be a Th2-driven disease. However, the histologic features of EGPA cannot be entirely explained by Th2 responses, and Th1 responses are thought to contribute to granuloma formation in EGPA.…”

Section: Pathophysiologymentioning

confidence: 99%

Eosinophilia in Rheumatologic/Vascular Disorders

Tamaki¹,

Chatterjee²,

Langford³

2015

Immunology and Allergy Clinics of North America

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“…T-cell lines from CSS patients generated in vitro by polyclonal stimulation are polarized toward a Th2 phenotype [32]. Clinically, it is evident that immunosuppressive therapy targeting lymphocytes is useful in treating CSS patients.…”

Section: Pathophysiologymentioning

confidence: 99%

Churg-Strauss syndrome: 2005–2008 update

Grau

2008

Curr Rheumatol Rep

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Churg-Strauss syndrome (CSS) is a rare necrotizing small-vessel vasculitis associated with eosinophil-rich granulomatous inflammation of tissues and vessels and is also associated with asthma and eosinophilia. Epidemiologic studies continue to show that CSS is the rarest of the necrotizing small-vessel vasculitides. However, it is not possible to know with any certainty if there has been an increase in incidence. There has been an attempt to divide the patients with CSS into an antineutrophil cytoplasmic antibody-positive and cytoplasmic antibody-negative group. The former group has an increased frequency of renal involvement, parenchymal pulmonary disease, constitutional symptoms, and peripheral and central nervous system involvement, whereas the latter group has more frequent cardiac disease. The role of eosinophils and antineutrophil cytoplasmic antibodies remains poorly defined but provocative. Leukotriene receptor antagonists do not appear to induce CSS but facilitate the tapering of glucocorticoids, which unmasks the condition. Glucocorticoids and cyclophosphamide remain the foundation of treatment for vasculitis, but there are other promising and less toxic alternatives on the horizon.

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Elevated interleukin-4 and interleukin-13 production by T cell lines from patients with Churg-Strauss syndrome

Cited by 138 publications

References 20 publications

Functional promoter polymorphism in the TBX21 gene associated with aspirin-induced asthma

Functional promoter polymorphism in the TBX21 gene associated with aspirin-induced asthma

Eosinophilia in Rheumatologic/Vascular Disorders

Churg-Strauss syndrome: 2005–2008 update

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