CTLA-4/CD 28 region polymorphisms in children from families with autoimmune hepatitis

Djilali-Saiah, Idriss; Ouellette, Patrice; Caillat‐Zucman, Sophie; Debray, Dominique; Kohn, Joaquin; Álvarez, Fernando

doi:10.1016/s0198-8859(01)00344-5

Cited by 57 publications

(29 citation statements)

References 37 publications

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“…Associations were found with BehÈet's disease and idiopathic ischemic stroke [8,9]. However, in accordance with our results, CD28 polymorphisms seemingly also do not influence susceptibility to various diseases, including autoimmune thyroid diseases and autoimmune hepatitis [53,54]. Lack of associations with PF were also observed for CD80 gene polymorphisms, in agreement with results reported for multiple sclerosis, rheumatoid arthritis, and systemic lupus erythematosus [10,12].…”

Section: Discussionsupporting

confidence: 91%

Polymorphisms in the 2q33 and 3q21 chromosome regions including T-cell coreceptor and ligand genes may influence susceptibility to pemphigus foliaceus

et al. 2010

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Section: Discussionsupporting

confidence: 91%

Polymorphisms in the 2q33 and 3q21 chromosome regions including T-cell coreceptor and ligand genes may influence susceptibility to pemphigus foliaceus

et al. 2010

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“…Polymorphisms outside the MHC have also been associated with autoimmune hepatitis [83], and they have included polymorphisms of the cytotoxic T lymphocyte antigen-4 gene (CTLA-4) [84,85], Fas gene (tumor necrosis factor receptor superfamily [TNFRSF] gene) [86,87], tumor necrosis factor-a (TNFA*2) gene [88][89][90], vitamin D receptor (VDR) gene [91,92], signal transducer and activator of transcription 4 (STAT4) gene [93], transforming growth factor beta 1 (TGF-b1) gene [94], and genes of various cytokines [95]. These polymorphisms have not been implicated in all ethnic populations of autoimmune hepatitis [96][97][98][99][100], and they have not been disease specific [101].…”

Section: Dig Dis Scimentioning

confidence: 99%

Transitioning from Idiopathic to Explainable Autoimmune Hepatitis

Czaja

2015

Dig Dis Sci

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Autoimmune hepatitis lacks an identifiable cause, and its diagnosis requires the exclusion of etiologically defined diseases that resemble it. Insights into its pathogenesis are moving autoimmune hepatitis from an idiopathic to explainable disease, and the goal of this review is to describe the insights that are hastening this transition. Two types of autoimmune hepatitis are justified by serological markers, but they also have distinctive genetic associations (DRB1 and DQB1 genes) and autoantigens. DRB1 alleles are the principal susceptibility factors in white adults, and a six amino acid sequence encoded in the antigen-binding groove of class II molecules of the major histocompatibility complex can influence the selection of autoantigens. Polymorphisms, including variants of SH2B3 and CARD10 genes, may affect immune reactivity and disease severity. The cytochrome mono-oxygenase, CYP2D6, is the autoantigen associated with type 2 autoimmune hepatitis, and it shares homologies with multiple viruses that might promote self-intolerance by molecular mimicry. Chemokines, especially CXCL9 and CXCL10, orchestrate the migration of effector cells to sites of injury and are associated with disease severity. Cells of the innate and adaptive immune responses promote tissue damage, and possible deficiencies in the number and function of regulatory T cells may facilitate the injurious process. Receptor-mediated apoptosis is the principal mechanism of hepatocyte loss, and cell-mediated and antibody-dependent mechanisms of cytotoxicity also contribute. Insights that explain autoimmune hepatitis will allow triggering exogenous antigens to be characterized, risk management to be improved, prognostic indices to be refined, and site-specific therapeutic interventions to emerge.

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“…There is a strong link to HLA-A1, -B8, -DR3, and -DRB1 to AIH [15,16,17]. Other polymorphisms of immunomolecules like CTLA-4 [18,19], CD45 [20], and TNF-α [21] have also been described in the context of AIH. T H 1 and T H 2 cytokines IFN-γ, IL-2, IL-4, and IL-6 are under discussion, but need further investigation.…”

Section: Requirements For Animal Models Reflecting Aihmentioning

confidence: 99%

Animal Models for Autoimmune Liver Disease – What Is Relevant for Immune-Mediated Liver Disease

Hardtke‐Wolenski

Taubert²,

Jaeckel³

2012

Dig Dis

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Autoimmune hepatitis (AIH) is a chronic autoimmune inflammation of the liver usually requiring lifelong immunosuppression. Steroids and azathioprine are the standard therapy, but the therapy is accompanied by strong side effects. Due to the fact that AIH is often recognized during the late course of disease, it is difficult to obtain knowledge about the immunological mechanisms responsible for initiation of the disease. Current AIH models have been helpful for understanding and modulating liver immune responses, but are not suited to study mechanisms in chronic AIH or to develop new therapies. While most common hepatitis models are more models of injury, transgenic AIH models deal with short-term hepatitis leading to tolerance, and models with natural antigens are either self-limited or have unknown target antigens. Therefore, new models with defined onset of AIH and a standardized course of disease are essential for a better understanding of the disease and to develop new therapies.

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CTLA-4/CD 28 region polymorphisms in children from families with autoimmune hepatitis

Cited by 57 publications

References 37 publications

Polymorphisms in the 2q33 and 3q21 chromosome regions including T-cell coreceptor and ligand genes may influence susceptibility to pemphigus foliaceus

Polymorphisms in the 2q33 and 3q21 chromosome regions including T-cell coreceptor and ligand genes may influence susceptibility to pemphigus foliaceus

Transitioning from Idiopathic to Explainable Autoimmune Hepatitis

Animal Models for Autoimmune Liver Disease – What Is Relevant for Immune-Mediated Liver Disease

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