There are some believers that think that atherosclerosis is an
infectious disease. Hence these cells may be responding to infection
of the endothelium. Most the recent literature concerns Chlamydia and
there are a number of good review articles out there. - Kevin Ault,
MD University of Iowa
Alec Redwood <aredwood at cyllene.uwa.edu.au> wrote:
>A question.
>T-cells are oftern seen in atherosclerotic lesions, they are also seen,
>to a lesser degree, in a process known as neo-intimal hyperplasia, which
>is seen in patients following vein grafts. There is some discussion
>that T-cells in atherosclerotic lesions are seeing some pathogen
>(although this is very debatable). However to the best of my knowledge
>there is no such evidence in neo-intimal hyperplasia (basically a
>thickening of the blood vessel wall as a result of smooth muscle
>proliferation). Certain models in nude and immunosuppressed (t-cell
>depleted or cylco A) rats show that T-cells can either increase or
>degrease neo-intimal hyperplasia.
>The question...more of a discussion actually
>What are they doing there? There is no evidence of an Ag (could it be
>self). If they are just by standers why do they have an effect? What
>activates them to produce IFN-gamma (as some suggest)... no Ag (and
>probably no second signal). This seems to be a forgoten area as many
>"healing" responses appear to have a T-cell component. Why are they
>there and how do they function...aparently outside their normal Ag
>sepecific role...In fact do they function in this role, is it all
>artifact.
>Any suggestions?
