Abstract:
: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.
journal_name
J Neuroimmunoljournal_title
Journal of neuroimmunologyauthors
Irani DNdoi
10.1016/s0165-5728(98)00038-1subject
Has Abstractpub_date
1998-07-01 00:00:00pages
11-6issue
1-2eissn
0165-5728issn
1872-8421pii
S0165-5728(98)00038-1journal_volume
87pub_type
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