Editorial |
From the Cardiovascular Research Unit, Center for Molecular Medicine, Karolinska Hospital, Stockholm, Sweden.
Correspondence to Sten Stemme, MD, PhD, Cardiovascular Research Unit, Center for Molecular Medicine L8:03, Karolinska Hospital, S-171 76 Stockholm, Sweden. E-mail sten.stemme@cmm.ki.se
The notion
that atherosclerosis has an inflammatory component was
already proposed in the 19th century by Virchow, on the basis of light
microscopic analysis of human plaques. The hypothesis was later
supported by electron microscopic studies and was confirmed when
immunohistochemical analysis revealed that the CD14+
macrophage indeed was the major cell type in the
plaque.1 2 More
surprising was the finding that T lymphocytes were also present in
substantial numbers in human
plaques.1 The presence of
cellular representatives of the specific, adaptive
immune system in this disease has since then inspired a whole area of
research, and our knowledge has certainly grown. T lymphocytes are
designed to perform effector functions after activation by a specific
antigen via the T-cell receptor. A first obvious question was,
therefore, what these antigen-specific cells might be reactive to. Are
there atherosclerosis-related antigens taking part in
atherogenesis? This inquiry constitutes something of a
"needle-in-a-haystack" problem, and the question of clonal
composition is easier to address. The presence of clonal T-cell
expansions would suggest reactivity to a limited number of antigens in
early experimental
atherosclerosis.3
More advanced human plaques, however, demonstrate a polyclonal T-cell
composition.4 5
This characteristic does not constitute evidence that T cells are
"nonspecific" (ie, are carrying reactivities not related to
atherosclerosis), but it does suggest that no single
antigen reactivity dominates the T-cell population. This result in
itself is not surprising, because it is known from other inflammatory
conditions, with known eliciting antigens, that antigen-specific cells
in general constitute a minority of all
|
ATVB Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2001 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |