Pathogens and autoimmune hepatitis

Abstract

Autoimmune hepatitis (AIH) is a severe form of hepatitis resulting in the autoimmune-mediated destruction of the liver parenchyma. Whereas many of the immunopathogenic events have been elucidated and some of the drivers of the disease have been identified, little is known about the aetiology of the disease. There are certain risk factors, such as particular human leucocyte antigen (HLA) haplotypes, that enhance the susceptibility for AIH or influence the severity of the disease. However, as for many other autoimmune diseases, the mere presence of such risk factors does not warrant the occurrence of the disease. Not all individuals carrying risk factors develop AIH, and not all patients with AIH are carriers of high-risk alleles. Thus, additional environmental factors need to be considered as triggers for AIH. Environmental factors include diet, sunlight exposure, stress, medication and hygiene, as well as pathogen infections and vaccinations. This review discusses if pathogens should be considered as triggers for the initiation and/or propagation of AIH.

Rescue of autoimmune hepatitis by soluble MHC class II molecules in an altered concanavalin A‐induced experimental model

“…Spleen cells were cultured in 96-well V-bottomed plates (Sarstedt, Numbrecht, Germany) at the concentration of 1 × 10 6 cells/well in DMEM culture medium (Biosera, Kansas City, USA) supplemented with 10% fetal bovine serum (FBS, Gibco) at a final volume of 200 μL with or without ConA 7,9 (1 μg/mL) and with or without sMHCII (30 ng/mL) 25 and processed for 3 HTdR incorporation assays after 4 days of culture as previously described. 22…”

Viral Infections and Autoimmune Disease: Roles of LCMV in Delineating Mechanisms of Immune Tolerance

“…It uses a similar approach as the RIP-LCMV model of autoimmune diabetes described above. More precisely, the GP or NP protein of LCMV is expressed in transgenic mice under the control of the albumin promoter (Alb) [11][12][13]. In contrast to RIP-LCMV mice however, Alb-LCMV mice develop transient hepatitis following infection with LCMV, due to the strong tolerogenic nature of the liver.…”

Viral Infections and Autoimmune Disease: Roles of LCMV in Delineating Mechanisms of Immune Tolerance<strong> </strong>

“…This model uses a similar approach as the RIP-LCMV model of autoimmune diabetes described above. More precisely, the GP or NP protein of LCMV is expressed in transgenic mice under the control of the albumin promoter (Alb) [12][13][14]. In contrast to RIP-LCMV mice, however, Alb-LCMV mice develop transient hepatitis following infection with LCMV due to the strong tolerogenic nature of the liver.…”