AbstractMouse thymocytes and erythrocytes form rosettes when incubated together at 4°. The frequency is much higher when the thymocytes and erythrocytes are MHC‐identical. If the indolizidine alkaloid swainsonine (SW) is present during rosette formation at concentrations of 1 μg/ml (5.7 μM) or greater, rosette formation between MHC‐identical pairs is inhibited to levels comparable to those observed for MHC‐different pairs: rosette formation by MHC‐different pairs is not affected. This was confirmed by examining 17 different MHC‐identical combinations (9 completely syngeneic and 8 differing in non‐MHC genes) and 13 MHC‐different combinations (3 of these identical everywhere except at MHC). A SW‐inhibitable component of rosette formation was observed only when thymocyte and erythrocyte were completely identical at MHC. Thus F1‐parent pairs behaved as if allogeneic, although both F1‐F1 and parent‐parent had a SW‐inhibitable rosetting component. Similarly, inbred strains only partially MHC‐identical (B10.BR‐B10.A, B10.D2‐B10.A) behaved as if allogeneic. The SW‐inhibitable component of rosetting could be partially but significantly blocked by including monoclonal antibodies against Thy‐1, and anti‐CD4 plus anti‐CD8(together but not separately); anti‐class‐l‐MHC produced some inhibition of marginal significance. Monoclonal antibodies against class‐l‐MHC, LFA‐1, and CD3 did not block. Pretreatment of erythrocytes with neuraminidase greatly reduced the SW‐inhibitable component of rosetting. The SW effect would appear to be due to a direct interaction of SW with a cell surface structure involved in syngeneic rosette formation rather than the known ability of SW to block the processing of N‐linked sugar structures. The results are consistent with cell surface lectins and
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