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1.
Scand J Rheumatol ; 45(2): 107-13, 2016.
Article in English | MEDLINE | ID: mdl-26926492

ABSTRACT

OBJECTIVES: In systemic sclerosis (SSc)-related interstitial lung disease (ILD), elevated eosinophil counts in bronchoalveolar lavage are associated with a worse outcome. We hypothesized that eosinophils may be activated in the peripheral circulation, thereby increasing their recruitment to affected tissues and contributing to inflammation and fibrosis. The aim of this study was to characterize the blood eosinophils in SSc patients. METHOD: Expression levels of surface markers CD11b, CD44, CD48, CD54, CD69, CD81, and HLA-DR on CD16(low)CD9(high)-expressing eosinophils were measured by flow cytometry in whole blood from SSc patients (n = 32) and controls (n = 11). RESULTS: Expression levels of CD54, CD69, and HLA-DR were undetectable in all groups. CD44 and CD11b expression levels were similar between groups. CD81 expression was lower in patients compared to controls independent of disease duration (p = 0.001). CD48 expression was increased in patients with a short disease duration (< 2 years) compared to both controls (p = 0.042) and patients with longer disease duration (≥ 2 years; p = 0.027). In patients with short disease duration, increased CD48 expression was associated with alveolar inflammation as measured by an increased concentration of alveolar nitric oxide (r = 0.76, p = 0.003). CONCLUSIONS: Blood eosinophils change phenotype during disease evolution in SSc, and CD48 expression may be used as a biomarker for pulmonary inflammation.


Subject(s)
Antigens, CD/metabolism , Eosinophils/metabolism , Pulmonary Fibrosis/metabolism , Scleroderma, Systemic/metabolism , Tetraspanin 28/metabolism , Aged , Biomarkers , CD48 Antigen , Case-Control Studies , Flow Cytometry , Humans , Male , Middle Aged , Nitric Oxide/metabolism , Phenotype , Pulmonary Fibrosis/etiology , Scleroderma, Diffuse/metabolism , Scleroderma, Limited/metabolism , Scleroderma, Systemic/complications , Time Factors
2.
Scand J Immunol ; 57(3): 203-13, 2003 Mar.
Article in English | MEDLINE | ID: mdl-12641648

ABSTRACT

The nonobese diabetic mouse is highly susceptible not only to diabetes but to several autoimmune diseases, and one might suspect that these are controlled by a shared set of genes. However, based on various gene-segregation experiments, it seems that only a few loci are shared and that each disorder is influenced also by a unique set of genes.


Subject(s)
Autoimmune Diseases/genetics , Mice, Inbred NOD/genetics , Animals , Autoimmune Diseases/immunology , Female , Genetic Predisposition to Disease , Genetic Variation/immunology , Major Histocompatibility Complex/genetics , Major Histocompatibility Complex/immunology , Male , Mice , Mice, Inbred NOD/immunology , Quantitative Trait Loci/immunology
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