Adult T cell leukemia: a tale of two T cells
O. John Semmes
O. John Semmes
Published April 3, 2006
Citation Information: J Clin Invest. 2006;116(4):858-860. https://doi.org/10.1172/JCI28140.
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Commentary

Adult T cell leukemia: a tale of two T cells

Abstract

Human T cell leukemia virus type 1 (HTLV-1) is the etiologic agent for the development of an aggressive hematologic neoplasia termed adult T cell leukemia/lymphoma (ATLL). Although the virus infects T cell subsets that display either CD4 or CD8 cell surface markers, the leukemic cell is exclusively of the CD4+ subtype. In the article by Sibon et al. in this issue of the JCI, the authors demonstrate that the molecular basis for clonal expansion differs between these 2 infected T cell populations (see the related article beginning on page 974). The molecular events associated with a preleukemic state, such as genomic instability, polynucleation, and cell cycle redistribution, were only observed in CD4+ T cells. This finding provides a molecular-based mechanism for the restriction of the leukemic phenotype to the CD4+ T cell subtype.

Authors

O. John Semmes

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Figure 1

HTLV-1 disease and clonal expansion of separate T cell subsets.

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HTLV-1 disease and clonal expansion of separate T cell subsets. After HT...
After HTLV-1 infection, both CD4+ and CD8+ T cell subpopulations exhibit clonal expansion. In this issue of the JCI, Sibon et al. (3) examined each subpopulation using a sophisticated ex vivo model system. The authors observed that although each infected cell type displayed clonal expansion, loss of genomic integrity, which is a necessary predisposition for neoplasia, was observed only in the CD4+ T cell population. Clonal expansion of the HTLV-1–infected CD8+ T cell population is associated with increased cell division and resistance to apoptosis. The interaction between the 2 molecular pathways toward clonal expansion utilized by each T cell subset could have significant impact upon which HTLV-1 disease will develop in an infected individual.