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Autoantibodies
in alopecia areata
In other autoimmune diseases autoantibodies can play an active
role in disease pathogenesis. Autoantibodies are produced by B
cells
of the immune system. They are small pieces of protein (glycoproteins)
which can recognize antigens. Autoantibodies recognize self antigens
and they can occasionally have very destructive activity. In all
forms of autoimmune disease an elevated production of antibodies
reactive with the target tissues is usually apparent and can be
organ specific, as in Hashimoto's thyroiditis where autoantibodies
only react with cells of the thyroid gland, or non-specific as
in
lupus where the autoantibodies can react with antigens found in
almost any cell. Autoantibodies can be extremely
destructive
as in Goodpastures syndrome where autoantibodies specific for
the kidney glomerular basement membrane cause kidney inflammation
and
eventual necrosis (permanent destruction). Autoantibodies
can have more unique activity as in thyrotoxicosis where thyroid
hyperactivity is the result of autoantibodies mimicking hormone
function by binding to cell surface thyroid hormone receptors.
Other autoantibodies can have no obvious effect at all. Most of
us, healthy or otherwise, have low levels of autoantibodies
in
our blood system but with no ill effects and even high levels
of autoantibodies in some autoimmune diseases have no obvious
activity.
Whether the antibodies produced are destructive or not depends
on their quality, quantity, and their specific antigen target.
Whatever
the importance of the autoantibodies in disease pathogenesis,
they are often used for their predictive value where detection
of certain
types in patient sera is regarded as diagnostic of certain diseases
(eg Scherbaum 1986a, Tan 1989).
Studies on autoantibodies in alopecia areata have been many
and the results conflicting. Some researchers conclude that the
presence
of autoantibodies to various organs is significantly elevated
in alopecia areata sufferers (Main 1975, Kern 1975, Schenk 1980,
Friedman
1981, Galbraith 1984, Zauli 1984) while others believe there is
no increased incidence of autoantibodies (Bettrele 1975, Cochran
1976, Muller 1980). Anti-nuclear antibodies (ANAs) have been found
in serum from alopecia areata sufferers by indirect immunofluorescence
(Schenk 1980, Nunzi 1980). Certain types of ANAs are associated
with such autoimmune diseases as lupus and rheumatoid arthritis.
Thyroid autoantibodies are significantly increased in people with
alopecia areata according to several
reports (Kern 1973, Friedman 1981, Galbraith 1984) along with
antibodies
against smooth muscle (Main 1975) and gastric parietal cells (Friedman
1981).
  
Pictures of anti-nuclear antibodies
Hair
follicle specific autoantibodies in alopecia areata
Attempts to detect autoantibodies against hair follicle components
in sera from alopecia areata patients have largely failed in the
past (eg Kern
1973, Friedman 1981, Muller 1980, Klaber 1978, Igarashi 1980).
However, more recent reports from several research groups provide
supporting evidence of hair folicle specific autoantibodies present
in people with alopecia areata (Calver 1992, Tobin 1994a, McElwee
1996). But it has also
been shown that low levels of hair follicle specific autoantibodies
can be found in sera from normal people. The significance
of anti-hair follicle autoantibodies in alopecia areata remains
to be elucidated, but their presence does suggest that an autoimmune
mechanism has been initiated (although an autoimmune mechanism
does not necessarily
mean an autoimmune disease is present).
   
Pictures of anti-hair follicle antibodies
Autoantibodies from B cells are just one route to autoimmune disease,
many other types of immune cell can be just as destructive. Considering
the majority of cells around lesional hair follicles in alopecia
areata are CD4+ and CD8+ lymphocytes these cells are possible alternative
candidates for being the initiators of alopecia areata.
Autoantibodies
in alopecia areata references
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Articles,
Links Smooth muscle antibodies and alopecia areata.
Br J
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