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Elevated interleukin‐4 and interleukin‐13 production by T cell lines from patients with Churg‐Strauss syndrome
Objective To investigate cytokine production patterns of T cell lines (TCL) from patients with Churg‐Strauss syndrome (CSS). Methods Short‐term polyclonal TCL were generated from peripheral blood of patients with CSS or Wegener's granulomatosis (WG) and healthy controls (HC). TCL were establish...
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Published in: | Arthritis and rheumatism 2001-02, Vol.44 (2), p.469-473 |
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Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites |
Online Access: | Get full text |
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Summary: | Objective
To investigate cytokine production patterns of T cell lines (TCL) from patients with Churg‐Strauss syndrome (CSS).
Methods
Short‐term polyclonal TCL were generated from peripheral blood of patients with CSS or Wegener's granulomatosis (WG) and healthy controls (HC). TCL were established in the presence of interleukin‐2 (IL‐2) and phytohemagglutinin and were phenotypically characterized by flow cytometry. Th1/Th2 cytokine production by stimulated TCL (72 hours) was analyzed by enzyme‐linked immunosorbent assay.
Results
TCL that represented the progeny of in vivo–activated T cells from CSS patients displayed a heterogeneous immunophenotype, with a predominance of CD4+ T cells when compared with WG TCL, which were predominantly CD8+. All CSS TCL shared the ability to produce large amounts of interferon‐γ (IFNγ), IL‐4, and IL‐13 compared with HC (P = 0.014 for all 3). Production of IL‐4 and IL‐13 was higher in CSS TCL than in WG TCL (P = 0.014 for both). IL‐5 production was up‐regulated in WG TCL compared with CSS TCL (P = 0.014). Compared with HC, WG TCL showed increased production of IFNγ (P = 0.021), IL‐5 (P = 0.043), and IL‐13 (P = 0.021).
Conclusion
Our results indicate that, while there is evidence for both a type 1 and a type 2 response in CSS, type 2 cytokine production pattern appears to predominate in this disease when compared with WG and HC. |
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ISSN: | 0004-3591 1529-0131 |
DOI: | 10.1002/1529-0131(200102)44:2<469::AID-ANR66>3.0.CO;2-0 |