Trained innate lymphoid cells in allergic diseases

Group 2 innate lymphoid cells (ILC2s) reside in peripheral tissues such as the lungs, skin, nasal cavity, and gut and provoke innate type 2 immunity against allergen exposure, parasitic worm infection, and respiratory virus infection by producing TH2 cytokines. Recent advances in understanding ILC2 biology revealed that ILC2s can be trained by IL-33 or allergic inflammation, are long-lived, and mount memorylike type 2 immune responses to any other allergens afterwards. In contrast, IL-33, together with retinoic acid, induces IL-10-producing immunosuppressive ILC2s. In this review, we discuss how the allergic cytokine milieu and other immune cells direct the generation of trained ILC2s with immunostimulatory or immunosuppressive recall capability in allergic diseases and infections associated with type 2 immunity. The molecular mechanisms of trained immunity by ILCs and the physiological relevance of trained ILC2s are also discussed

Gastric duplication complicated by hypergastrinemia: A case report

Introduction: Gastrointestinal duplications are rare congenital anomalies that can occur anywhere throughout the intestinal tract. However, gastric duplication is very rare. A case of gastric duplication with uncommon complications, hypergastrinemia and duodenal ulcer, is described. Case report: The patient was an 11-year-old girl who presented with epigastric pain and non-bilious vomiting. The patient had a history of recurrent duodenal ulcers. Gastrin levels when the patient first presented with a duodenal ulcer at 8 years of age had reached 730 pg/mL. Computed tomography (CT) showed a cyst outside the pyloric antrum after remission of the duodenal ulcer, and it was suspected to be gastric duplication. For recurrence of the duodenal ulcer, the patient had been treated with histamine 2 receptor blockade for 3 years. At 11 years of age, the patient had stopped the medication and presented with gastric pain and vomiting. CT showed an enlarged gastric cyst and an obstructed pylorus. The patient was then referred to our hospital, and a laparotomy was performed to resect the cyst. Histological examination revealed positive staining for gastrin in the cyst wall mucosa, which is consistent with gastric duplication. Postoperative serum gastrin levels decreased, suggesting that gastric duplication had caused the hypergastrinemia. Conclusion: A case of gastric duplication was presented. Gastric duplication should be considered when treating patients with cystic disease of the pyloric region. In addition, hypergastrinemia may occur due to duplicated intestine near the pylorus, which may cause a duodenal ulcer