Direct characterization of human T cells in pemphigus vulgaris reveals elevated autoantigen-specific Th2 activity in association with active disease

C. Rizzo, M. Fotino, Y. Zhang, S. Chow, A. Spizuoco, A. A. Sinha

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59 Scopus citations

Abstract

Pemphigus vulgaris (PV) is a blistering skin disorder mediated by autoantibodies targeting the epidermal adhesion molecule desmoglein 3 (Dsg3). As Th2-associated cytokines are necessary for directing antibody production, it is hypothesized that Dsg3-specific Th2 activity is associated with active disease. We used cell-surface-matrix technology in combination with flow cytometry to characterize the Dsg3-reactive T-cell population using peripheral blood mononucleocytes sampled from PV patients stratified by active (n = 9) or remittent disease (n = 6), and healthy human leucocyte antigen-matched controls (n = 5). We evaluated interferon-γ-producing CD4+ cells (Th1) and interleukin (IL)-10- or IL-4-producing CD4+ cells (Th2). The mean frequency of Th2 CD4+ T cells was significantly elevated for five of nine PV patients with active disease. No significant Th2 responses were detected for patients with remittent disease or controls. There was a significant association of Th2 activity with active disease compared with remittent and control groups (P = 0.026 and P = 0.012, respectively), and Th2 activity was significantly correlated with anti-Dsg3 IgG titre (P = 0.044). One patient with remittent disease converted from a Th2-negative to a Th2-positive response with the initiation of disease activity. An antigen-specific CD4-lymphocyte response was detected in five PV patients (36%), and was shown to correlate closely with the CD8+ population. These results are consistent with the hypothesis that Th2 response directs autoantibody production and is therefore associated with disease activity in PV.

Original languageEnglish
Pages (from-to)535-540
Number of pages6
JournalClinical and Experimental Dermatology
Volume30
Issue number5
DOIs
StatePublished - Sep 2005
Externally publishedYes

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