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Duodenal lymphocytosis, sometimes called lymphocytic duodenitis, lymphocytic duodenosis, or duodenal intraepithelial lymphocytosis, is a condition where an increased number of intra-epithelial lymphocytes is seen in biopsies of the duodenal mucosa when these are examined microscopically.
Intraepithelial lymphocytes (IEL) are lymphocytes found in the epithelial layer of mammalian mucosal linings, such as the gastrointestinal (GI) tract and reproductive tract. [1] However, unlike other T cells, IELs do not need priming. Upon encountering antigens, they immediately release cytokines and cause killing of infected target cells.
The treatment of lymphocytic esophagitis is still undefined. [5] Treatment either targets symptoms, inflammation or complications. For example, heartburn is a symptom in lymphocytic esophagitis, and proton pump inhibitors , which reduce acidity in the stomach, are consequently used for treatment.
Intraepithelial lymphocytes interspersed into epithelial layer of mucosal surfaces; Lymphoid aggregates in the appendix and large intestine; Mesenteric lymph nodes draining lymph coming from the gut tissue; GALT can be also divided into two categories considering the structure, from which the function arise.
EATL arises from the malignant transformation of small-intestinal intraepithelial lymphocytes (IEL). IEL are a heterogeneous group of principally T-cell lymphocytes residing in epithelial tissues that interface the environment, such as the mucosa of the bronchi, reproductive tract and gastrointestinal tract. [6]
In contrast, γδ T cells have a TCR that is made up of one γ (gamma) chain and one δ (delta) chain. This group of T cells is usually less common than αβ T cells. Their highest abundance is in the gut mucosa, within a population of lymphocytes known as intraepithelial lymphocytes (IELs). [1]
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More recent studies of adults with autoimmune enteropathy expanded the criteria to include prolonged diarrhea (lasting longer than six weeks) accompanied by malabsorption, diminished intraepithelial lymphocytosis, deep crypt lymphocytosis, increased crypt apoptotic bodies, and the exclusion of other causes of villous atrophy; each of the ...
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