Abnormal expression of the low‐affinity receptor for inter‐leukin‐2 (IL‐2R) is a characteristic of the HTLV‐I (+) leukemic T cells in adult T‐cell leukemia (ATL). Despite the expression of IL‐2R bearing Tac antigen (IL‐2R/pSS), leukemic cells of the majority of ATL patients do not proliferate in response to IL‐2. In the human NK cell line, YT, as well as in ATL‐derived T cells, the co‐expression of IL‐2R/p55 and the second IL‐2R without the Tac epitope (IL‐2R/p70) is required to produce high‐affinity IL‐2R. To study the effect of HTLV‐I on both of the IL‐2Rs, we transferred a fragment of HTLV‐I containing the p40X gene into YT cells. One of the 2 transfected YT clones (YT/pX‐5.1) had an increased level of expression of IL‐2R/p55. In contrast, expression of (L‐2R/p70 was unaffected, as determined by Scatchard analysis and the cross‐linking study using 125‐IL‐2. Our results show that the T‐cell phenotype is not required for induction of IL‐2R/p55 by p40X. We suggest that HTLV‐I infection induces a disproportionate induction of IL‐2R/pSS without significant enhancement of IL‐2R/p70 expression, resulting in the predominant expression of low‐affintty IL‐2R in ATL. IL‐2R/p70 may be a critical parameter determining the IL‐2 reactivity of HTLV‐I‐infected T cells as well as of normal lymphocytes.
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