1. In vivo anti-tumor activity of CD3-AK cells. (A). CD3-AK cells were induced by activation of mouse splenocytes with alphaCD3-AK antibody. The conventional LAK cells were induced by activation of mouse splenocytes with purified human recombinant IL-2. We found that different tumors showed different degrees of susceptibility to the in vivo killing by CD3-AK or LAK cells and the results also correlated with the in vivo effect of the killer cells on these tumors. A plasmacytoma P815 was much-more susceptible to the killing by CD3-AK than by LAK cells, and the in vivo growth of P815 cells was inhibited by simultaneous inoculation of CD3-AK and was not affected by LAK cells. In contrast, a melanoma JBMS was susceptible to the killing by LAK but was resistant to - CD3-AK mediated killing, and the in vivo growth of JBMS was retarded by LAK cells and was not affected by CD3-AK. Due to the ability of CD3-AK to expand rapidly in vitro, CD3-AK may be an attractive candidate for immunotherapy of susceptible tumors. 2. Mechanisms for lymphocyte-mediated cytolysis. (B). Two subsets of killer cells were induced by alphaCD3. The killer cells that were maintained in IL2 and alpha-CD3 (CD3-AK+) induced fast lysis, whereas the killer cells that were maintained in IL-2 alone induced slow lysis. Protein kinase C (PKC) was not required in fast lysis but was required in slow lysis. Cytolytic granules might be involved in fast lysis but had very little effect in slow lysis. On the other hand, cytokines such as IL-2, IL-4 and TNF were involved in slow lysis but had no effect in fast lysis.
