**1. Introduction**

Celiac disease (CD) is a systemic disorder of an autoimmune nature that occurs in genetically susceptible individuals. It is caused by gluten and related prolamins and is characterised by the presence of a variable combination of gluten-dependent clinical manifestations, the presence of CD-specific antibodies, along with genetics compatible with HLA-DQ2 or HLA-DQ8 haplotypes and the presence of varying degrees of enteropathy [1].

It is triggered by the consumption of foods that contain or are made with gluten, mainly through wheat proteins (gliadins), and also rye (secalins), barley (hordeins) and certain varieties of oats (avenins).

It is a chronic disease with a genetic basis that affects, or may affect, various organs and systems in which inflammation of the small intestine may lead to various symptoms and eventually to malabsorption of nutrients. Treatment of CD consists of permanently following a gluten-free diet (GFD), which was developed in 1951 by the Dutch paediatrician Dr. Willem Karel Dicke, in the course of treating children suffering from chronic diarrhoea with malnutrition who had been admitted to the Children's Hospital of Utrecht after the Second World War. He found that they improved when foods containing wheat flour were removed from the diet. This was the starting point for the introduction of the GFD, which is the only treatment for CD that is effective throughout the world, and it has been applied ever since [2].

Genetics, immunology and aspects of the environment are important factors in the development of CD. Its principle determinants are the class II genes of the HLA system, which are largely related to the presence of HLA-DQ2 and HLA-DQ8 [3]. It is primarily an immune disorder, mediated by T cells, that affects the intestinal mucosa of genetically predisposed individuals. CD4+ T cells recognise gluten peptides, which are selectively present in the context of the molecules HLA-DQ2(+) and DQ8(+) [4].

The enzyme transglutaminase 2 (TG2) deaminates positively charged gluten peptides. Gluten-specific CD4+ T cells, such as the cytotoxic intraepithelial CD8 T lymphocytes, play an important role in the development of intestinal lesions. Gluten is the most important environmental factor involved in its development, but other environmental factors have been implicated, such as infections, dysbiosis and exposure to drugs [5, 6].

The Consensus Conference of Experts Meeting in 2012 and 2013, celebrated in Oslo and London respectively have accurately described the terms related to CD and also the sensitivity to non-celiac gluten sensitivity (NCGS) and wheat allergy, to unify criteria and accurately define the differences between such disorders [7, 8].
