leew at wadsworth.org
Thu Feb 23 13:06:58 EST 1995
In article <9501237935.AA793556122 at WRSMTP-CCMAIL.ARMY.MIL> dr._jack_komisar at WRSMTP-CCMAIL.ARMY.MIL ("dr. jack komisar") writes:
>From: dr._jack_komisar at WRSMTP-CCMAIL.ARMY.MIL ("dr. jack komisar")
>Subject: Re: Superantigens
>Date: 23 Feb 1995 05:13:03 -0800
> Many superantigens stimulate CD4 and CD8 T cells, even
> though presentation on MHC class II antigens is required for
> a positive reaction in most assay systems.
> Staphylococcal enterotoxin A (SEA) is the most potent T
> cell mitogen known. As few as 1-5 molecules can activate a
> human T cell.
> Jack Komisar
What is the basis for CD8 reactivity? I've seen a couple of papers showing
activation of T cells by sAg in the absence of APCs although more papers (and
our own experiments) indicate an absolute requirement. Does this depend on
the sAg (we almost always use SEB)? Also some paers have shown that there is a
requirement for B7 expression/interaction for sAg stimulation. If there is
direct activation in the absence ofAPCs, then I can understand CD8
activation--you get direct binding to the TcR. If APCs are required, it's
a little harder to explain, unless the sAg has affinity for class I. Most of
the papers I've seen on CD8 expansion have been from in vivo-treated mice.
Has CD8 activation been observed in vitro with pure cell poulations? Could
the CD8 expansion be due to some bystander effect (plus direct some signal
from direct TcR binding) due to the massive IL-2 production from the CD4
cells? Also, this is anecdotal, but if you prime a mouse with SEB and look at
the spleen, you see expnasion of VB8 cells plus vb8 CD8's. But it seems as
if most of the increase in total cellularity is due to non-T cells. In short,
there'e a lot of stuff going on and CD4's are not the only cell type going.
But what is going with the CD8'c mechanistically?
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