The changing face of chronic autoimmune atrophic gastritis: an updated comprehensive perspective

Chronic autoimmune atrophic gastritis (CAAG) is an organ-specific autoimmune disease, which affects the corpus–fundus gastric mucosa. Although it has been described for several years, the real pathophysiological mechanisms, the natural history and the possible neoplastic complications are not completely known. Atrophy of the gastric mucosa is the endpoint of the chronic processes, with the loss of glandular cells and their replacement by intestinal-type epithelium, pyloric-type glands, and fibrous tissue. As a consequence, hydrochloric acid, pepsin and intrinsic-factor is impaired resulting in pernicious anemia. The exact causal agent is not yet known, but both genetic and environmental factors seem to play a decisive role.Moreover, the clinical onset may assume different characteristics; differently from what previously observed, recent evidence has reported the onset of CAAG at a younger age, frequently with iron deficiency anemia or upper gastro-intestinal symptoms.The diagnosis of CAAG might be challenging and usually requires the combination of clinical, serological and histopathologic data; moreover, CAAG patients are often misdiagnosed as refractory to HP eradication therapy, probably because achlorhydria might allow urease-positive bacteria other than H pylori to colonize the stomach, causing positive ¹³C-urea breath test results.However, biopsy is the most reliable method to evaluate the presence of metaplastic atrophic gastritis. In order to assess the severity of gastric atrophy and intestinal metaplasia, OLGA and OLGIM staging systems have been proposed and seem to correlate with the risk of developing gastric adenocarcinoma. Indeed, CAAG represents a pre-neoplastic condition, as patients with CAAG are very likely to develop either type-1 gastric neuroendocrine tumors and gastric adenocarcinomas, as well as several other neoplastic diseases. To date, the need, the intervals and cost-effectiveness of endoscopic/histological surveillance for patients with CAAG/pernicious anemia are yet to be established.     

Helminths products directly modulate T cells that mediate experimental autoimmune encephalomyelitis

Infection with helminths can protect against the development of autoimmune diseases and this has been associated with induction of anti‐inflammatory innate immune responses and Tregs. Here, we demonstrate that helminth‐derived products can directly target T cells, especially IL‐17‐secreting γδ T cells that play a key pathogenic role in CNS autoimmune disease.     

Are rats more human than mice?

In contrast to rats, mouse models are nowadays generally used for the investigation of immune responses and immune-mediated diseases, there are many different strains and mouse-specific tools available, and it is easy to generate transgenic and constitutive or inducible knockout mice for any gene. Many immune markers and mechanisms have been detected in mice and have been introduced as gold standard in immunology, however, some turned out to be not unconditionally transferable to the human immune system.Rats have been used more frequently in former days but are mostly outstripped by mice due to the fact that fewer strains are available, they need more space than mice, are more expensive to maintain and breed, and it is extremely difficult to generate transgenic or ko-rats. Consequently, the choice of rat-specific diagnostic tools like antibodies is quite poor and most researchers have switched to mouse models for the investigation of immune mechanisms, while rats are still widely used for toxicology by the pharmaceutical industry. However, it should be taken into consideration that there are some immunological similarities between rats and humans that are not presented in mice. Some of them like MHC class II and Foxp3 expression by activated effector T cells we have detected during our research on the immune response of rat models of experimental autoimmune uveitis.     

IgG4相关性甲状腺疾病研究的最新进展

免疫球蛋白相关性疾病(immunoglobulin G4- related diseases,IgG4- RD)可累及全身各个器官,累及甲状腺者称为IgG4相关性甲状腺疾病(IgG4- related thyroid disease,IgG4- RTD)。其临床特点为受累器官弥漫性或局灶性肿大、硬化,血清IgG4升高。部分IgG4- RD可导致器官衰竭,特别是胰腺、肝脏和胆道、肾脏、甲状腺、肺和主动脉等。IgG4- RTD多表现为甲状腺局部结节或弥漫性肿大,多伴有血清IgG4升高。IgG4- RTD目前病因未明,多认为与遗传因素、病毒感染、抗原抗体反应有关,治疗上绝大多数对糖皮质激素治疗有效。本文概述了近年来IgG4相关性甲状腺疾病的研究进展。