Tumor growth and adherence change the expression of macrophage Mac-2.

The galactose-specific animal lectin, Mac-2, has been identified in macrophage (M phi) membrane, cytoplasmic, and nuclear fractions. Flow cytometric analyses showed that there is a decrease in membrane Mac-2 during tumor growth. After 24-h adherence there was an increase in the number of normal host (NH) and tumor-bearing host (TBH) Mac-2+ M phi. Immunoblot analyses of NH and TBH M phi identified changes in the subcellular localization of Mac-2. The increase in nuclear Mac-2 during tumor growth, and after prolonged adherence of NH and TBH M phi, correlates with an increase in M phi entering the late G1 phases of the cell cycle. Northern blot analyses showed an increase in Mac-2 mRNA during tumor growth, and an increase in NH and TBH M phi after 24-h adherence. Tumor growth is able to manipulate the immune system through M phi by causing a down-regulation in membrane Mac-2 and an up-regulation in intracellular Mac-2. NH and TBH M phi respond to adherence by expressing increased membrane and nuclear Mac-2, but TBH M phi response is lower.