Abstract
In this report, we found that an anti-CD44 mAb, S5, augmented conjugate formation between the effector cells (canine PBMC) and an NK-sensitive target cell line [canine thyroid adenoma carcinoma cell line (CTAC)], as determined by two different methods: conjugate enumeration using fluorescence microscopy and two-color flow cytometric analysis. However, no increase in conjugate formation was seen when an NK-resistant target was used. This enhancement of initial conjugate formation could not be blocked using an antibody to CD18 (60.3), indicating that S5 possibly acted through another adhesive molecule(s). But the NK killing activity can be partially blocked by 60.3, indicating that this molecule may be important for later adhesive events. We also found that S5 stimulated the release of a heat labile cytotoxic factor from canine PBMC. This factor was found to lyse only TNFα-sensitive targets (CTAC and L929 cell lines) and caused apoptosis in the target cells. Its bioactivity was neutralized by polyclonal antibody to TNFα. All of these observations were consistent with the fact that the factor was TNFα Our data suggested that the two mechanisms responsible for the enhancement in canine NK activity by an mAb to CD44 were an increase in conjugate formation and the release of TNFα.
Published Version
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