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The gastrointestinal system
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Sharon J. White, Francis A. Carey
Coeliac disease is the most common intestinal cause of malabsorption in the Western world. It affects about 1 in 2,000 individuals in the UK, but 1 in 300 in the west of Ireland. The condition usually presents in infancy or early childhood, but may become manifest only in adult life. It is due to a genetically determined, abnormal cell-mediated immune response to gliadin, a derivative of the wheat protein gluten (hence its alternative name gluten-sensitive enteropathy). There is a strong familial tendency and an association with HLA-B8. The skin disease dermatitis herpetiformis is also associated with HLA-B8, and most patients with this skin disease appear also to have coeliac disease.
Gastroenterology
Published in Paul Bentley, Ben Lovell, Memorizing Medicine, 2019
Predisposing: HLA-B8, -DR8Autoimmunity Scleroderma, dermatomyositis, rheumatoid arthritis, Sjögren (in 80%)Addison, coeliac, vitiligo, Hashimoto, pulmonary fibrosis
Non-viral liver disease
Published in Michael JG Farthing, Anne B Ballinger, Drug Therapy for Gastrointestinal and Liver Diseases, 2019
John ML Christie, Roger WG Chapman
Severity of the inflammation, judged both biochemically and histologically, can predict prognosis. In addition, HLA type predicts outcome. Serum aspartate aminotransferase (AST) and gammaglobulin levels are the most useful biochemical test; serum AST level of over 10 times normal predicts a 10-year mortality of 90%. HLA B8 and DR3 identify younger patients with more severe inflammation and less response to corticosteroid therapy and greater frequency of liver transplantation. HLA DR4 patients tend to be older, female and respond better to treatment than patients with DR3.65
What’s new and what’s next for biological and targeted synthetic treatments in psoriatic arthritis?
Published in Expert Opinion on Biological Therapy, 2022
Flavia Sunzini, Arianna D’Antonio, Mauro Fatica, Paola Triggianese, Paola Conigliaro, Elisabetta Greco, Alberto Bergamini, Maria Sole Chimenti
Both human leukocyte antigen (HLA) and non-HLA genes have been associated with PsA and/or PsO. Among the HLA genes, HLA-B27 is associated with the axial involvement, and HLA-C*0602 associated with PsO and, to a lesser extent, to PsA [6]. Interestingly, different HLA genes, including HLA-B*08, B*27, B*38, and B*39, have been linked to different clinical manifestations in PsA [7]. Genome-wide association studies (GWAS) linked non-HLA genes with PsA pathogenesis, including molecules involved in the immune activation and signaling, such as type I interferons (IFNs), tumor necrosis factor (TNF)-α, and interleukin (IL)-23/IL-17 pathways. For example, IL-23 R, IL-23A (p19), IL-12B (p40), tyrosine kinase 2 (TYK2), TRAF3 Interacting Protein 2 (TRAF3IP2) have been consistently associated with PsA [8,9].
An inflammatory triangle in Sarcoidosis: PPAR-γ, immune microenvironment, and inflammation
Published in Expert Opinion on Biological Therapy, 2021
Parnia Jabbari, Mona Sadeghalvad, Nima Rezaei
Sarcoidosis is a polygenic disorder, and several genes with different phenotypes are associated with disease development. Although further investigations are needed to determine, certain HLA-alleles have been distinguished to influence susceptibility to sarcoidosis [29]. In 2009, Grunewald J et al. showed that HLA- DRB1*03 (DR3) allele is associated with Löfgren syndrome, a type of acute sarcoidosis. In their study, 301 patients with Löfgren syndrome were included, and the significant association was found between HLA-DR3 allele and disease recovery within 2 years. However, 49% of HLA-DR3 negative patients developed a non-resolving disease [30]. In addition, HLA-DRB1*15 (DR15) and DRB1*14 (DR14) have been recognized to be associated with chronic non-resolving disease [31]. It has been mentioned that among the patients with sarcoid arthritis, HLA-B8 and HLA-B14 are more prevalent alleles and HLA-DRB1*04 is considerably rare. These patients are also carriers for HLA-DR3 allele [7].
Prophylactic and therapeutic strategies for Epstein–Barr virus-associated diseases: emerging strategies for clinical development
Published in Expert Review of Vaccines, 2019
Vijayendra Dasari, Debottam Sinha, Michelle A. Neller, Corey Smith, Rajiv Khanna
Another prophylactic vaccine strategy tested in a phase I clinical trial was primarily designed to control the expansion of EBV-infected B cells by inducing a T-cell response to EBV latent antigens [57–59]. This vaccine was formulated with an EBNA3A peptide epitope (FLRGRAYGL) restricted through human leukocyte antigen (HLA)-B*08:01 with tetanus toxoid in a water-in-oil emulsion, Montanide ISA 720. Of the 14 enrolled seronegative HLA-B*08:01+ subjects, four received placebo, two were immunized with a high dose (50 µg) of EBNA3A peptide and the remaining eight were immunized with a low dose (5 µg) of peptide. Out of the nine evaluated volunteers, eight developed a T-cell response to EBNA3A peptide after vaccination. Subsequently, after 2–12 years of follow-up, two of the four placebo recipients became EBV infected and one developed IM. Interestingly, four of the eight vaccine recipients who received low-dose vaccine seroconverted, but none developed IM. In the high-dose vaccine group, one of the two subjects seroconverted and developed mild cases of IM [59]. Although the cohort is too small to draw any conclusions on the role of T-cell immunity in controlling IM, it clearly demonstrates the feasibility of vaccination and protection against IM in healthy volunteers.