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Defective Expression of IL‐2 Receptors on Peripheral Blood Lymphocytes from Patients with Cluster Headache
Author(s) -
Martelletti R,
Stirparo G.,
Stefano L.,
Sabato F.,
Giacovazzo M.,
RinaldiGaraci C.
Publication year - 1990
Publication title -
headache: the journal of head and face pain
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.14
H-Index - 119
eISSN - 1526-4610
pISSN - 0017-8748
DOI - 10.1111/j.1526-4610.1990.hed3004228.x
Subject(s) - transferrin receptor , receptor , cd16 , il 2 receptor , cd3 , microbiology and biotechnology , interleukin 2 , monoclonal antibody , receptor expression , cytotoxic t cell , immunology , lymphoblast , incubation , cd8 , biology , antigen , antibody , medicine , immune system , t cell , in vitro , cell culture , biochemistry , genetics
SYNOPSIS In a previous study we demonstrated that cluster headache (CH) patients present an increased Natural Cytotoxic response after incubation of their peripheral blood lymphocytes (PBL) with Interleukin‐2 (IL‐2). This phenomenon led to an investigation of the phenotypic expression of PBL before and after IL‐2 incubation, and of the IL‐2 lymphocyte receptor. IL‐2 receptor is expressed on T‐lymphocytes activated with an high‐affinity binding site. The analysis of the function of human IL‐2 receptor was facilitated by the production of a specific monoclonal antibody (MAb). This MAb identifies the IL‐2 receptors by blocking the binding of radiolabelled IL‐2 to T‐cells. In addition, we studied the expression of Leu‐4, specific for T‐cells; of Leu‐11b, specific for FC receptor on NK cells; and the Transferrin Receptor, specific for lymphoblasts and monocytes. Twenty‐three episodic CH patients were selected for this study. Ten sex and age‐matched healthy volunteers were used as the control group. We evaluated the PBL phenotypic expression of cells subsets before incubation with IL‐2 (1,000 I.U./ml) and after 72 hours. The following Becton Dickinson MAbs have been used: anti‐Leu‐4 (CD3), anti‐lL‐2 receptors (CD25), anti‐Transferrin receptor (TFR) and anti‐Leu‐11b (CD16). Indirect fluorescence with a Becton Dickinson FACS‐420 flow cytometer was used to analyze the cells. The results showed no significant variations in Leu‐4, Leu‐11b and Transferrin receptor in PBL of CH patients when compared to those of control subjects, both before and after incubation with IL‐2, whereas the percentage of PBL expressing receptors for IL‐2 was markedly reduced in CH patients as compared to normal individuals after incubation with IL‐2. This defective expression of IL‐2 receptors seems to be independent of the cluster period. These data suggest that the failure of IL‐2 receptor expression in CH can be inserted into a complex network of abnormalities of the immunoneuromodulating system in this disease.