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Induction of apoptosis seems to be a main function of these receptors. It is astonishing that a member of this family, CD30, is overexpressed by highly proliferating tumours such as Hodgkin lymphoma (HL) and anaplastic large cell lymphoma (ALCL). It is known that CD30 stimulation leads to the apoptosis of ALCL tumour cells but not of Hodgkin\u2013Reed\u2013Sternberg (HRS) cells. We have already established the overexpression of TRAF1 in HRS cells. In this study we demonstrate that A20 is highly expressed in the HRS cells in 20\/22 of cases of classical HL, in 4\/4 cases of nodular lymphocyte\u2010predominant HL (NLPHL), and in 2\/2 cases of the anaplastic variant of diffuse large B cell lymphoma. In contrast, all other non\u2010Hodgkin lymphomas, including ALCL, revealed either no A20 reactivity, or reactivity in less than 1% of all tumour cells. CD30 stimulation induced A20 and TRAF1 expression. This effect was most prominent in HL and ALCL cell lines with low basal expression levels of these molecules. Immunohistological studies of reactive lymphoid blasts in tonsillar tissue demonstrated that co\u2010expression of CD30, A20, and TRAF1 also occurs <jats:italic>in vivo<\/jats:italic>. Cell lines with high basal A20 and TRAF1 expression were resistant to CD30\u2010mediated apoptosis. The sensitivity to CD30\u2010induced apoptosis was increased by inhibition of protein synthesis. TRAF1 transfection decreased CD30\u2010induced apoptosis. Our data suggest that A20 and TRAF1 contribute to apoptosis resistance and, therefore, play an important role in the pathogenesis of classical HL. 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