Human T-cell leukemia virus type-I-infected T-cell lines scarcely produce p56lck, whether or not they express lck mRNA.

We have previously reported that lck mRNA (a lymphocyte-specific protein tyrosine kinase gene) is absent in human T-cell leukemia virus type I (HTLV-I)-infected interleukin-2(IL-2)-independent T-cell lines, while HTLV-I-negative T-cell lines and HTLV-I-positive IL-2-dependent ones express a large amount of lck mRNA. To further investigate the levels of lck expression, we prepared rabbit anti-Lck antiserum directed against the synthetic oligopeptide of 32 amino acids corresponding to the carboxy terminus of this gene product, p56lck. Using this antiserum, we show that HTLV-I-positive T-cell lines, whether they are IL-2-dependent or not, scarcely express p56lck. In other words, IL-2-dependent HTLV-I-positive T-cell lines seldom produce p56lck in spite of high expression of lck mRNA. Absence of p56lck is suspected of playing an important role in malignant transformation of HTLV-I-infected T-cells.