by the National Academy of Sciences
ABSTRACT In the last few years, data from experiments employing
transgenic models of autoimmune diseases have strengthened a particular
concept of autoimmunity: disease results not so much from cracks
in tolerance induction systems, leading to the generation of an
, as from the breakdown of secondary systems
that keep these cells in check.
T cells with
anti-self specificities are readily found in disease-free individuals
but ignore target tissues. This is also the case in some
transgenic models, in spite of overwhelming numbers of autoreactive cells.
In other instances, local infiltration and inflammation result, but
they are well tolerated for long periods of time and do not
terminally destroy target tissue. We review the possible molecular and
cellular mechanisms that underlie these situations, with a particular emphasis
on the destruction of pancreatic beta cells in transgenic models of insulin-dependent
diabetes.
medicina de família crm 41.521 |
+19 3256 9968 |
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