ANCA and ASCA Profiles in a Moroccan Population With Inflammatory Bowel Diseases.

Introduction: Diagnosing inflammatory bowel disease (IBD) is hindered by the invasive procedures required for accurate classification as Crohn's disease (CD) or ulcerative colitis (UC). As alternatives, non-invasive tests using anti- antibodies (ASCA) and anti-neutrophil cytoplasmic antibodies (ANCA) have gained significance. This study evaluated ANCA and ASCA antibody frequencies in IBD and their role in disease characterization in a Moroccan population.

Inborn errors of immunity and related microbiome.

Inborn errors of immunity (IEI) are characterized by diverse clinical manifestations that are dominated by atypical, recurrent, chronic, or severe infectious or non-infectious features, including autoimmunity, lymphoproliferative disease, granulomas, and/or malignancy, which contribute substantially to morbidity and mortality. Some data suggest a correlation between clinical manifestations of IEI and altered gut microbiota. Many IEI display microbial dysbiosis resulting from the proliferation of pro-inflammatory bacteria or a decrease in anti-inflammatory bacteria with variations in the composition and function of numerous microbiota.

Anti-double stranded DNA antibodies: A rational diagnostic approach in limited-resource settings.

Context: Anti-double-stranded deoxyribonucleic acid antibodies (dsDNA Abs) are highly specific markers of systemic lupus erythematosus (SLE). Multiple methods are employed for their detection in routine diagnostics.

Objectives: The aim of this study was to evaluate a diagnostic approach for anti-dsDNA Abs using DNA-ELISA and fluorescence test (CLIFT), in combination with antinuclear antibody (ANA) screening.

[Autoimmune hepatitis: Immunological diagnosis].

Autoimmune hepatopathies (AIHT) including autoimmune hepatitis (AIH), primary biliary cirrhosis (PBC), primary sclerosing cholangitis (PSC) and autoimmune cholangitis (AIC), represent an impressive entities in clinical practice. Their pathogenesis is not perfectly elucidated. Several factors are involved in the initiation of hepatic autoimmune and inflammatory phenomena such as genetic predisposition, molecular mimicry and/or abnormalities of T-regulatory lymphocytes.