Soluble CD30 and peripheral blood or pulmonary involvement of adult T-cell leukemia/lymphoma

Abstract

Adult T-cell leukemia/lymphoma (ATL) is a highly aggressive leukemia/lymphoma which was discovered in Japan [1,2]. The long clinical latency and low incidence of ATL indicate that ATL is an agerelated disease and some genetic changes are involved in malignant transformation and monoclonal expansion of the human T-cell leukemia virus type 1 (HTLV-1)-infected cells [3]. HTLV-1-mediated T-cell transformation presumably arises from a multistep oncogenic process in which the virus induces chronic T-cell proliferation with accumulation of genetic defects followed by dysregulation of cell growth [4]. Monoclonal proliferation of HTLV-1-infected cells is observed in upwards of 5% of patients who ultimately develop ATL, constituting the high risk group for ATL development [5]. We previously reported that HTLV-1-infected cells and ATL cells exhibit CD30 and soluble CD30 (sCD30) is elevated in the sera of patients with ATL [6]. CD30, a 120 kDa type I cell surface glycoprotein, is a member of the tumor necrosis factor receptor superfamily [7]. CD30 expression is dependent on mitogen or viral activation and proliferation of B and T cells. CD30+ cells release sCD30 in vitro and in vivo [8], detected at low levels in the sera of healthy donors [9].The question remains as to where the ATL cells proliferate and produce sCD30? We have focused on the monoclonal proliferation of T cells and chronic inflammation in the microenvironment in vivo.