I need an exact, full-detail picture of current knowledge on both celiac
sprue and tropical sprue.  There are "big" implications if things fit
together in a certain way.  For right now, I want to get updated.  Please
make any additions or corrections to the story I tell below.  Direct email
is welcome, and likewise invitations to communicate any other way.  Part of
the problem you'll see with this is that my immunology is 20 years out of
date, and I was never good at histology.

THE STORY--
Celiac sprue is a collapse of small-intestine function triggered by
ingestion of 'gluten,' any of a number of cereal proteins.  The intestinal
mucosa on biopsy show "flattened" texture and an abundance of invasive
immune cells (anyone able to tell me what cell types are observed?).  When
the disease is active, patients have "anti-endomysial antibodies" in their
blood (in operational terms, a slice of monkey esophagus is exposed to
patient's serum, then to fluorescent monkey anti-human antibody.
Fluorescence is observed in muscular regions of the slice.  I'm told that
there's also a test using human umbilical cord--can someone explain it to
me?  A peculiarity seen is that many victims of celiac disease produce no
IgA heavy chains, so the test must be done with monkey antibodies which are
also sensitive to IgM).

It has been found that digestion of glutens with stomach and pancreatic
enzymes leaves a 33-unit peptide which binds readily to cellular
transglutaminase (and can be attached to other proteins by the action of
transglutaminase).  While anti-endomysial antibodies are a complex mixture,
antibodies against c-transglutaminase are a major component (a fly in the
ointment is that the test for the mixture correlates better with celiac
disease than a test for anti-transglutaminase alone).  It has been suggested
that cellular transglutaminase is recognized by precursors of
antibody-producing cells, but that in the maturation of the immune system,
lines of helper cells which would promote the action of those cells are
eliminated.  When several proteins, including transglutaminase, are
decorated with the gluten-derived peptide, helper cells primarily reacting
to the presence of the foreign peptide also promote production of antibodies
against transglutaminase and other assorted inappropriate targets.  This
need for cross-promotion fits with the observation that celiac sprue is
strongly associated with certain HLA types.  (Please help me with exact cell
types, by the way--I could fill them in for the general case, but I remember
that intestinal immunity is special).

Transglutaminase in the cell membrane is needed for the formation of cell
layers on basement membrane, fitting with the loss of villous structure on
biopsy.  Invasion of the intestinal mucosa by immune cells would follow from
the presence of antibodies bound to mucosal cells.

Assorted further observations on celiac sprue: symptoms generally resolve in
about a month when gluten is completely removed from the diet.  Most cases
in which disease persists turn out to be complicated by lymphoproliferative
conditions.  Sensitive tests of brain activity have shown multi-focal areas
of inactivity during times of gluten exposure in celiac sprue patients.  The
nutrients not absorbed in these conditions are principally carbohydrates and
vitamins (especially the water soluble vitamins); protein and fat absorption
are impaired less.

Tropical sprue is a collapse of small-intestine function seen in those who
have resided in certain tropical areas.  Outbreaks occur, distinct in time
and location.  Duration tends to be several years, but treatment with
antibiotics and niacin generally produces improvement in less than a month
and resolution in less than six months.  The intestinal mucosa on biopsy are
indistinguishable from specimens from celiac sprue, but the patients' blood
contains no endomysial antibodies.  The cause is not known.

Long story, and I want you to make it longer for me (and correct the
outright howlers, PLEASE).  A foreshadowing of what I'm getting at is that I
have the barest hint of a reason to suppose that the final disease-causing
process in celiac sprue and tropical sprue may be the same.  This would make
anti-endomysial antibodies something of a red herring (although a
diagnostically convenient one).