TCR rearrangement in patients with eosinophilic lung disease

Nathalie Freymond , Vincent Cottin, Chahéra Khouatra , Jean-Emmanuel Kahn, Nadia Sivova, Lionel Prin , Fanny Legrand, Jean-François Cordier

Author address: 

National Reference Center for Rare Pulmonary Diseases, Louis Pradel Hospital, Lyon, France; Department of Internal Medicine, Foch Hospital, Suresnes, France; Immunology Laboratory, University Hospital, Lille, France

Abstract: 

Background: Expansion of monoclonal population of T-cells with T-cell receptor (TCR) rearrangements and aberrant cell surface immunophenotype produce IL-5 and contribute to the pathophysiology of the lymphocytic variant of the hypereosinophilic syndrome (HES). Objective: To characterise T-cell expansion in eosinophilic lung disease. Methods: T-cell expression profile was analysed by flow cytometry and TCR clonal gene rearrangements were studied by PCR in 45 consecutive patients with peripheral blood eosinophilia (greater than 1.0x 109/L) and eosinophilic lung disease. Patients with myeloid or lymphocytic variants of HES or any identified cause of eosinophilia were excluded. Results: Clonal TCR rearrangements were detected in 11/45 patients (24%): 4/18 with hypereosinophilic asthma, 3/17 with Churg-Strauss syndrome, 3/9 with idiopathic chronic eosinophilic pneumonia (ICEP), and 1/1 with allergic bronchopulmonary aspergillosis. Seven patients had 2 clonal rearrangements or more. TCR rearrangements involved the TCRγ chain in 10 patients and the TCRδ chain in one patient with ICEP. Aberrant T-cell immunophenotype usually found in HES (CD3-CD4+, CD3+CD4-CD8-, or CD3+CD7)- , and known to produce IL-5, was not detected. No significant clinical or biological difference was found between patients with or without clonal TCR gene rearrangements. IL-5 serum level was normal in all patients. Conclusion: Expansion of TCR-Vγ or TCR-Vδ populations are present in a proportion of patients with eosinophilic lung disease without aberrant cell-surface immunophenotype. Further study is needed to evaluate whether T-cell clonality might contribute to the pathophysiology of these conditions or is only a transient reactive phenomenon.
2011

abstract No: 

P1835

Full conference title: 

European Respiratory Congress
    • ERS 21st (2011)