The Role of HLA in the Association between IgA Deficiency and Celiac Disease
Poddighe D. Capittini C.
2021Hindawi Limited
Disease Markers
2021#2021
Selective IgA deficiency (SIgAD) is the most frequent primary immune defect. Since SIgAD is not characterized by relevant infectious issues in most cases, it is often diagnosed during the diagnostic work up of several and different autoimmune disorders, which are associated with this primary immune defect. The genetic background of SIgAD is complex and three HLA haplotypes resulted to be more frequently associated with it; in detail, two of them include HLA-DQB1∗02 allelic variants, which are essential predisposing factors to develop Celiac Disease (CD). Here, we discuss the evidence regarding the role of HLA in the etiopathogenesis of SIgAD and its association with CD. Actually, the HLA region seems to play a modest role in the genetic predisposition to SIgAD and we may speculate that the association with the HLA-DQB1∗02 alleles (or haplotypes including them) could derive from its link with CD. Indeed, SIgAD and some related immunological alterations are likely to predispose to several autoimmune diseases (with and despite different HLA backgrounds), including CD, which is relatively common and directly associated with the HLA-DQB1∗02 allelic variants coding the DQ2 heterodimer. Further and specific studies are needed to make final conclusions in this regard.
Text of the article Перейти на текст статьи
School of Medicine, Nazarbayev University, Nur-Sultan, Kazakhstan
Clinical Academic Department of Pediatrics, National Research Institute for Maternal and Child Health, University Medical Center, Nur-Sultan, Kazakhstan
Clinical Epidemiology and Biometric Unit, Scientific Direction, IRCCS Policlinico San Matteo Foundation, Pavia, Italy
School of Medicine
Clinical Academic Department of Pediatrics
Clinical Epidemiology and Biometric Unit
10 лет помогаем публиковать статьи Международный издатель
Книга Публикация научной статьи Волощук 2026 Book Publication of a scientific article 2026