Intraepithelial lymphocytes (IEL) are lymphocytes found in the epithelial layer of mammalian mucosal linings, such as the gastrointestinal (GI) tract and reproductive tract. However, unlike other T cells, IELs do not need priming. Upon encountering antigens, they immediately release cytokines and cause killing of infected target cells. In the GI tract, they are components of gut-associated lymphoid tissue (GALT).

An elevated IEL population, as determined by biopsy, typically indicates ongoing inflammation within the mucosa. In diseases such as celiac sprue, IEL elevation throughout the small intestine is one of many specific markers.

Alternatively, elevated IEL populations can be a marker for developing neoplasia in the tissue such as found in cervical and prostate cancers, as well as some colorectal cancers, particularly those associated with Lynch syndrome (hereditary non-polyposis colon cancer ). IELs themselves can, when chronically activated, undergo mutation that can lead to lymphoma.

Gluten-sensitive enteropathy–associated conditions are comorbidities or complications of gluten-related gastrointestinal distress (that is, gluten-sensitive enteropathy or GSE). GSE has key symptoms typically restricted to the bowel and associated tissues; however, there are a wide variety of associated conditions. These include bowel disorders (diarrhoea, constipation, irritable bowel), eosinophilic gastroenteritis and increase with coeliac disease (CD) severity. With some early onset and a large percentage of late onset disease, other disorders appear prior to the celiac diagnosis or allergic-like responses (IgE or IgA, IgG) markedly increased in GSE. Many of these disorders persist on a strict gluten-free diet (GF diet or GFD), and are thus independent of coeliac disease after triggering. For example, autoimmune thyroiditis is a common finding with GSE.

However, GSEs' association with disease is not limited to common autoimmune diseases. Coeliac disease has been found at increased frequency on followup to many autoimmune diseases, some rare. Complex causes of autoimmune diseases often demonstrates only weak association with coeliac disease. The frequency of GSE is typically around 0.3 to 1% and lifelong risk of this form of gluten sensitivity increases in age, possibly as high as 2% for people over 60 years of age. This coincides with the period in life when late-onset autoimmune diseases also rise in frequency.

Genetic studies indicate that coeliac disease genetically links to loci shared by linkage with other autoimmune diseases. These linkages may be coincidental with how symptomatic disease is selected from a largely asymptomatic population.

Primary biliary cirrhosis. CD is prevalent in primary biliary cirrhosis (PBC). In PBC anti-mitochondrial antibodies are directed toward 3 mitochondrial autoantigens (pyruvate dehydrogenase, oxoglutarate dehydrogenase, branched-chain alpha-keto acid dehydrogenase), 2 or more nuclear proteins (nucleoporin 210kDa, nucleoporin 62kDa, centromere protein, and sp100), and 57% of acute liver failure patients have anti-transglutaminase antibodies.

Cholangitis. CD also found at higher than expected frequencies in autoimmune cholangitis and primary sclerosing cholangitis. CD is frequently linked to pancreatitis but also to papillary stenosis and, in India, tropical calcific pancreatitis appears also to be associated with CD.

Oat sensitivity represents a sensitivity to the proteins found in oats, "Avena sativa". Sensitivity to oats can manifest as a result of allergy to oat seed storage proteins either inhaled or ingested. A more complex condition affects individuals who have gluten-sensitive enteropathy in which there is also a response to avenin, the glutinous protein in oats similar to the gluten within wheat. Sensitivity to oat foods can also result from their frequent contamination by wheat, barley, or rye particles.

Studies on farmers with grain dust allergy and children with atopy dermatitis reveal that oat proteins can act as both respiratory and skin allergens. Oat dust sensitivity in farms found 53% showed reactivity to dust, second only to barley (70%), and almost double that of wheat dust. The 66 kDa protein in oats was visualized by 28 out of 33 sera (84%). However, there was evident non-specific binding to this region and thus it may also represent lectin-like binding. IgA and IgG responses, meanwhile, like those seen to anti-gliadin antibodies in celiac disease or dermatitis herpetiformis, are not seen in response to avenins in atopic dermatitis patients. Food allergies to oats can accompany atopy dermatitis. Oat avenins share similarities with γ and ω-gliadins of wheat — based on these similarities they could potentiate both enteropathic response and anaphylactic responses. Oat allergy in gluten-sensitive enteropathy can explain an avenin-sensitive individual with no histological abnormality, no T-cell reaction to avenin, bearing the rarer DQ2.5"trans" phenotype, and with anaphylactic reaction to avenin.