Brain-derived gangliosides induce cell cycle arrest in a murine T cell line

Gangliosides modulate various T cell effector functions through poorly defined mechanisms. To begin to understand one of their effects, the present study examined how normal brain-derived gangliosides suppress T cell proliferation using the murine T cell line, EL4, as a model. Gangliosides inhibited EL4 cell growth by causing progressive cell cycle arrest. Dephosphorylation of the retinoblastoma protein (pRB) appeared to be the principal mechanism through which this effect was produced. Since okadaic acid could reverse both the growth arrest and pRB dephosphorylation, gangliosides may activate a phosphatase to mediate these events. Taken together, these data have implications for understanding how the local proliferation of T cells exposed to endogenous gangliosides within the brain may be regulated.