Autoimmune gastritis (AIG) is a non-self-limiting, chronic, inflammatory disorder of the stomach which causes progressive atrophy of the oxyntic mucosa, leading to vitamin B12, iron and other micronutrients deficiencies. Although recent advances have been made in understanding its epidemiology, pathophysiology and clinical aspects, there remains gaps in knowledge which need to be filled. In particular, the natural history of AIG needs to be better defined, as well as factors triggering autoimmunity, and key mucosal players which trigger mucosal atrophy. The significance and role of anti-parietal cell antibodies in causing AIG are still uncertain. Additionally , factors leading to neoplastic complications, namely gastric type I neuroendocrine tumours and adenocarcinoma, are poorly described.
The goal of this research topic is to provide novel insights into the pathogenesis and clinical aspects of AIG. In particular, studies regarding mucosal immunology (at both molecular and cellular levels), the role of disease-specific antibodies (anti-intrinsic factor, anti-parietal cell antibodies and others) and the natural history (i.e., from the potential phase to the complicated or neoplastic phase) are welcome.
Any type of article is welcome (excluding brief research reports), although original articles are preferred. We welcome submissions based on these topics, but not limited to:
• Adaptive and innate immunological mechanisms leading to autoimmune gastritis in murine models or humans
• T-cell dependent apoptotic mechanisms leading to gastric atrophy
• Role and significance of auto-antibodies in autoimmune gastritis
• From atrophy to cancer: mechanisms of neuroendocrine or epithelial carcinogenesis in autoimmune gastritis
Autoimmune gastritis (AIG) is a non-self-limiting, chronic, inflammatory disorder of the stomach which causes progressive atrophy of the oxyntic mucosa, leading to vitamin B12, iron and other micronutrients deficiencies. Although recent advances have been made in understanding its epidemiology, pathophysiology and clinical aspects, there remains gaps in knowledge which need to be filled. In particular, the natural history of AIG needs to be better defined, as well as factors triggering autoimmunity, and key mucosal players which trigger mucosal atrophy. The significance and role of anti-parietal cell antibodies in causing AIG are still uncertain. Additionally , factors leading to neoplastic complications, namely gastric type I neuroendocrine tumours and adenocarcinoma, are poorly described.
The goal of this research topic is to provide novel insights into the pathogenesis and clinical aspects of AIG. In particular, studies regarding mucosal immunology (at both molecular and cellular levels), the role of disease-specific antibodies (anti-intrinsic factor, anti-parietal cell antibodies and others) and the natural history (i.e., from the potential phase to the complicated or neoplastic phase) are welcome.
Any type of article is welcome (excluding brief research reports), although original articles are preferred. We welcome submissions based on these topics, but not limited to:
• Adaptive and innate immunological mechanisms leading to autoimmune gastritis in murine models or humans
• T-cell dependent apoptotic mechanisms leading to gastric atrophy
• Role and significance of auto-antibodies in autoimmune gastritis
• From atrophy to cancer: mechanisms of neuroendocrine or epithelial carcinogenesis in autoimmune gastritis
