Allergen-induced CD30 expression on T cells of atopic asthmatics

Summary Background The importance of TH2‐type T cell cytokines in atopic disease is widely accepted. CD30, a member of the TNF/NGF receptor superfamily, is expressed on a proportion of activated CD45RO+ T cells and has been proposed as a marker for TH2 phenotype. CD30 ligand‐CD30 interaction has been shown to positively influence development of the TH2 phenotype, and serum levels of soluble CD30 (sCD30) have been used as prognostic markers in HIV, SLE, Epstein‐Barr Virus infection and Hodgkin's Lymphoma but not as yet in allergic disease. Objectives To establish if serum levels of sCD30 are elevated in atopic asthma and determine whether allergen‐induced proliferation/activation of PBMCs from atopic asthmatics promotes CD30 expression on CD4+ T lymphocytes. Further, to determine if expression of CD30 and sCD30 correlate with disease severity. Methods Eighteen atopic asthmatics were each assigned a symptomatic disease score based on symptoms and bronchodilator rescue usage. Serum sCD30 was measured in peripheral blood by ELISA. PBMCs from atopic asthmatics were analysed with flow cytometry to obtain the proportions of CD4 T cells expressing CD45RO and CD30. The cells were then cultured for 10 days with IL‐2 with or without house dust mite antigen. A proliferation index was recorded and expression of CD30 and CD45RO retested. As a control, stimulation with PHA was used. Results with patients’ PBMCs were compared with results of a parallel analysis of PBMCs from non‐atopic healthy controls. Results Serum sCD30 was elevated in the 18 atopic asthmatics compared with a group of normal subjects but levels did not correlate with symptomatic disease activity. CD4CD45RO expression was low (14%) in atopic asthmatic peripheral blood but increased to 41% after 10 days culture with allergen. The CD4:CD8 ratio increased after Der p stimulation. A significant rise in the percentage of CD44 T cells expressing surface CD30 (29%) was seen along with increased mean fluorescence intensity. Both these results correlated with symptomatic disease severity score. Non‐specific PHA stimulation failed to significantly affect CD30 expression. Conclusions There is a specific response to allergen in atopic asthma which causes significant increases in CD30 expression. This may correlate with disease severity.