Immunity, inflammation and disease · 2022
The modulation of macrophage subsets in celiac disease pathogenesis.
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Molaaghaee-Rouzbahani Sara, Asri Nastaran, Jahani-Sherafat Somayeh, Amani Davar, Masotti Andrea, Baghaei Kaveh, Yadegar Abbas, Mirjalali Hamed, Rostami-Nejad Mohammad
Аннотация
BACKGROUND: So far, limited studies have focused on the role of Macrophages (MQs) in the development or progression of celiac disease (CD). Researchers believe that increasing knowledge about the function of MQs in inflammatory disorders plays a critical role in finding a new treatment for these kinds of diseases.
MAIN BODY: CD is a permanent autoimmune intestinal disorder triggered by gluten exposure in predisposed individuals. This disorder happens due to the loss of intestinal epithelial barrier integrity characterized by dysregulated innate and adaptive immune responses. MQs are known as key players of the innate immune system that link innate and adaptive immunity. MQs of human intestinal lamina propria participate in maintaining tissue homeostasis, and also intestinal inflammation development. Previous studies suggested that gliadin triggers a proinflammatory phenotype (M1 MQ) in human primary MQs. Moreover, M2-related immunosuppressive mediators are also present in CD. In fact, CD patients present an impaired transition from pro-inflammatory to anti-inflammatory responses due to inappropriate responses to gliadin peptides.
CONCLUSION: The M1/M2 MQs polarization balancing regulators can be considered novel therapeutic targets for celiac disease.
MAIN BODY: CD is a permanent autoimmune intestinal disorder triggered by gluten exposure in predisposed individuals. This disorder happens due to the loss of intestinal epithelial barrier integrity characterized by dysregulated innate and adaptive immune responses. MQs are known as key players of the innate immune system that link innate and adaptive immunity. MQs of human intestinal lamina propria participate in maintaining tissue homeostasis, and also intestinal inflammation development. Previous studies suggested that gliadin triggers a proinflammatory phenotype (M1 MQ) in human primary MQs. Moreover, M2-related immunosuppressive mediators are also present in CD. In fact, CD patients present an impaired transition from pro-inflammatory to anti-inflammatory responses due to inappropriate responses to gliadin peptides.
CONCLUSION: The M1/M2 MQs polarization balancing regulators can be considered novel therapeutic targets for celiac disease.