Interleukin-13 responsiveness and interleukin-13 receptor expression in non-Hodgkin's lymphoma and reactive lymph node B cells. Modulation by CD40 activation

• Published in: European cytokine network (Montrouge) Vol. 8; no. 1; p. 19
• Main Authors: Billard, C, Caput, D, Vita, N, Ferrara, P, Orrico, M, Gaulard, P, Boumsell, L, Bensussan, A, Farcet, J P
• Format: Journal Article
• Language: English
• Published: France 01.03.1997
• Subjects: B-Lymphocytes - drug effects; B-Lymphocytes - metabolism; CD40 Antigens - metabolism; Cell Division; Humans; Interleukin-13 - pharmacology; Interleukin-13 Receptor alpha1 Subunit; Lymph Nodes - cytology; Lymph Nodes - drug effects; Lymph Nodes - metabolism; Lymphoma, Non-Hodgkin - metabolism; Receptors, Interleukin - metabolism; Receptors, Interleukin-13
• ISSN: 1148-5493

Interleukin-13 (IL-13) responsiveness was examined in lymph node B cells from patients with non-Hodgkin's lymphoma (NHL) and patients with benign reactive immune disorders. Proliferation assays showed that NHL B cells from 8 of 21 patients responded to IL-13 in the absence of a co-activation signal. IL-13-unresponsive NHL B cells from 9 of the 13 remaining patients were induced to respond to IL-13 upon antibody-triggered CD40 activation, as did reactive B cells. Binding experiments with radiolabeled IL-13 revealed that the constitutive expression of IL-13 receptors (IL-13R) was associated with IL-13 responsiveness in the absence of CD40 activation. In IL-13-unresponsive cells, IL-13R expression was induced after CD40 activation. This effect was enhanced by IL-10, which was able to potentiate the IL-13 response of CD40-activated cells. Furthermore, IL-13 was found to increase the viability of cultured NHL cells, but not that of non-malignant cells. These results suggest that IL-13, which behaves as a potent co-factor for normal lymph node B cell activation, might provide growth and/or survival advantages to NHL B cells.