The present study was undertaken in order to determine whether the expression of specific surface molecules which mediate immune recognition as well as cell-cell and cell-matrix interactions is associated with the leukemic evolution of T-cell lymphomas. To this end, we have investigated the in vivo phenotypic characteristics and the in vitro natural-killer(NK)-cell susceptibility of a group of MCF-247-induced AKR/J T-cell lymphomas with different leukemic potential. We found that in the AKR/J model, the biological aggressiveness of leukemic cells is not dependent upon an escape from host immune surveillance as a consequence of an in vivo down-regulation of H2-K(k) determinants or a resistance to NK lysis. Moreover, NK susceptibility of AKR/J lymphomas does not seem to correlate with the level of H2-antigen expression. No obvious correlation was found between the leukemic phenotype and the amount of MEL-14, LFA-I, ICAM-I, Pgp-I/CD44 and THAM/CD26 antigen expression. An in vivo coordinated up-regulation of α4 and β7 integrin chains, with the highest levels of expression detected in secondary sites of leukemic infiltration, was observed in the highly leukemic lymphoma NQ22 and, albeit to a lesser extent, in lymphomas with moderate leukemic potential. Conversely, non-leukemic lymphomas were repeatedly α4- and β7-negative. These findings suggest that in the AKR/J system the expression of α4 β7 integrin may contribute to leukemic spreading of T- cell lymphomas.
|Number of pages||8|
|Journal||International Journal of Cancer|
|Publication status||Published - 1994|
ASJC Scopus subject areas
- Cancer Research