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Rebecca Carruthers
Physiology 410
Dr. Weichhaus
Celiac Disease
Writing assignment I
Cause:
Mechanistically celiac disease is a small intestinal mucosal injury and nutrient malabsorption in
people with a genetic predisposition when ingesting proline, glidans and glutanine rich proteins
found in gluten products (1). People who have celiac disease have an immune response that
attacks the small intestine when ingesting gluten, the trigger for this attack is called gliadin (2).
When immune cells attack the cells in the small intestine the villi in the small intestine are
damaged and the body can not absorb nutrients properly (2). This happens when gliadan resists
degradation and binds with a secretory IgA in the mucosal membrane of the small intestine (3).
Instead of being destroyed like most things bound to secretory IgA, transferrin receptors are over
expressed in the gut cells (epithelial cells) and the gliadan binds (3). Once it binds it makes it
through the gut epithelial cells and into the main propria or the lining on the gut wall (3). The
tissue transglutamate, then removes an amide in gliadan, and the deaminated glidans are then
eaten by macrophages which are serving the glidans on a MHC II (Major Histocompatibility
Complex) which are determined by HLA genes to pick what they serve and then the immune
system checks them out (3). The T-Helper cells then pick up the glidan and release inflammatory
cytokines which hurt the villi in the small intestine (3). This response initiates B-Cells to be
released which pump out anti Glidan, anti-tTG and anti-endomysial, which help with diagnosis
(3). Then the killer T-Cells destroy inflated cells, thus destroying the villi and letting more gliadin
into the gut lining (3). The damage mostly occurs in the duodenum or the first third of the small
intestine anatomically (3). This disease is called an autoimmune disease that leads to
malnourishment and if left untreated can cause several other autoimmune diseases and
complications (4).
Celiac disease is a genetic disorder that can be triggered by stressful events. Human
leukocyte antigen (HLA) class II genes as mentioned earlier in the mechanistic overview known
as HLA-DQ2 and HLA-DQ8 present antigens to the immune cells and are required for the
disease to materialize (5). These genes are on chromosome 6 and are very complex genes because
different alleles determine disease risk and these HLA peptide bindings play the main role in
