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Blood, Vol. 94 No. 1 (July 1), 1999:
pp. 275-282
Expression of the Human Immunodeficiency Virus-Tat Gene in Lymphoid
Tissues of Transgenic Mice Is Associated With B-Cell Lymphoma
Ramendra K. Kundu,
Frank Sangiorgi,
Lan-Ying Wu,
Paul K. Pattengale,
David R. Hinton,
Parkash S. Gill, and
Robert Maxson
From the Departments of Biochemistry and Molecular Biology,
Pathology, and Medicine, University of Southern California School of
Medicine, the USC/Norris Hospital and Research Institute, Los Angeles,
CA.
The human immunodeficiency virus type 1 (HIV-1) Tat gene, a potent
transactivator of viral and cellular genes, has been proposed as a key
agent in the pathogenesis of acquired immune deficiency syndrome
related disorders, including nonHodgkin's lymphoma. In cultured cells,
the HIV-1 Tat protein can induce the expression of the cytokines
interleukin-6 (IL-6) and IL-10, which are known to induce proliferation
and differentiation of lymphoid cells. Such alterations in cytokine
expression, together with a secondary genetic event, are thought to
ultimately lead to oncogenic transformation. To address the influence
of Tat on lymphoid development in the context of the whole organism, we
produced several transgenic mouse lines that express the Tat gene under
the control of an actin promoter. We show here that this promoter
directs expression to a variety of sites, including spleen, bone
marrow, and lymph nodes. Approximately 25% to 30% of the
Tat-transgenic population developed enlarged spleens within 1 year
after birth. On histological examination, a significant number of
spleens from Tat-transgenic mice exhibited malignant lymphoma of B-cell
origin. IgG heavy chain rearrangement confirmed the clonal B-cell
nature of these lymphoproliferations. In contrast, T-cell receptor
genes exhibited a germline (unrearranged) structure. Reverse
transcription polymerase chain reaction analysis of transgenic spleens
revealed that mRNA encoding cytokines IL-6 and IL-10 was upregulated,
suggesting a possible mechanism for the B-cell expansion in vivo.
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