Major depressive disorder(MDD)is a prevalent psychiatric disease that involves malfunctions of different cell types in the brain.Accumulating studies started to reveal that microglia,the primary resident immune cells,...Major depressive disorder(MDD)is a prevalent psychiatric disease that involves malfunctions of different cell types in the brain.Accumulating studies started to reveal that microglia,the primary resident immune cells,play an important role in the development and progression of depression.Microglia respond to stress-triggered neuroinflammation,and through the release of proinflammatory cytokines and their metabolic products,microglia may modulate the function of neurons and astrocytes to regulate depression.In this review,we focused on the role of microglia in the etiology of depression.We discussed the dynamic states of microglia;the correlative and causal evidence of microglial abnormalities in depression;possible mechanisms of how microglia sense depression-related stress and modulate depression state;and how antidepressive therapies affect microglia.Understanding the role of microglia in depression may shed light on developing new treatment strategies to fight against this devastating mental illness.展开更多
Leptin, a protein hormone produced by the adipocytes, has long been recognized to regulate metabolism, neuroendorine and other physiological functions. Early findings of increased leptin production during infection an...Leptin, a protein hormone produced by the adipocytes, has long been recognized to regulate metabolism, neuroendorine and other physiological functions. Early findings of increased leptin production during infection and inflammation and dysregulated immune response in leptin signaling-deficient mice provide strong evidence for the involvement of leptin in the immune responses. Recent data have established the regulatory function for leptin in immunity similar to the function of a pro-inflammatory cytokine, while gene-targeting studies also demonstrated an essential role of leptin in regulating hematopoiesis and lymphopoiesis. Moreover, there has been increasing evidence that leptin is involved in the pathogenesis of various autoimmune diseases. This review discusses recent advances in understanding the role of leptin in immunity and leptin-signaling pathways involved in modulating immune homeostasis and autoimmune pathogenesis. Cellular ＆ Molecular Immunology. 2007;4（1）：1-13.展开更多
Within the interleukin-17 （IL-17） family of cytokines, IL-17A is known to be critical in the host defense against fungal infections; however, the function of the other IL-17 family members in anti-fungal immunity re...Within the interleukin-17 （IL-17） family of cytokines, IL-17A is known to be critical in the host defense against fungal infections; however, the function of the other IL-17 family members in anti-fungal immunity remains largely unknown. Here, we show that IL-17C expression was highly induced in kidney epithelial cells after fungal infection. Mice that lacked IL-17C exhibited increased survival and attenuated kidney tissue damage, although they had similar fungal loads. IL-17C deficiency resulted in decreased pro-inflammatory cytokine expression compared with wild-type control mice. Additionally, IL-17C directly acted on renal epithelial cells in vitro to promote pro-inflammatory cytokine production. Taken together, our data demonstrate that IL-17C is a critical factor that potentiates inflammatory responses and causes host injury during fungal infection.展开更多
基金supported by the National Natural Science Foundation of China(31830032,81527901,and 31671057)the non-profit Central Research Institute Fund of the Chinese Academy of Medical Sciences(2017PT31038,2018PT31041)+3 种基金the National Key Research and Development Program of China(2016YFA0501000)Key-Area Research and Development Program of Guangdong Province(2018B030334001,2018B030331001)the 111 Project(B13026)the Fountain-Valley Life Sciences Fund of University of Chinese Academy of Sciences Education Foundation and the CAMS Innovation Fund for Medical Sciences(2019-I2M-5-057)。
文摘Major depressive disorder(MDD)is a prevalent psychiatric disease that involves malfunctions of different cell types in the brain.Accumulating studies started to reveal that microglia,the primary resident immune cells,play an important role in the development and progression of depression.Microglia respond to stress-triggered neuroinflammation,and through the release of proinflammatory cytokines and their metabolic products,microglia may modulate the function of neurons and astrocytes to regulate depression.In this review,we focused on the role of microglia in the etiology of depression.We discussed the dynamic states of microglia;the correlative and causal evidence of microglial abnormalities in depression;possible mechanisms of how microglia sense depression-related stress and modulate depression state;and how antidepressive therapies affect microglia.Understanding the role of microglia in depression may shed light on developing new treatment strategies to fight against this devastating mental illness.
文摘Leptin, a protein hormone produced by the adipocytes, has long been recognized to regulate metabolism, neuroendorine and other physiological functions. Early findings of increased leptin production during infection and inflammation and dysregulated immune response in leptin signaling-deficient mice provide strong evidence for the involvement of leptin in the immune responses. Recent data have established the regulatory function for leptin in immunity similar to the function of a pro-inflammatory cytokine, while gene-targeting studies also demonstrated an essential role of leptin in regulating hematopoiesis and lymphopoiesis. Moreover, there has been increasing evidence that leptin is involved in the pathogenesis of various autoimmune diseases. This review discusses recent advances in understanding the role of leptin in immunity and leptin-signaling pathways involved in modulating immune homeostasis and autoimmune pathogenesis. Cellular ＆ Molecular Immunology. 2007;4（1）：1-13.
文摘Within the interleukin-17 （IL-17） family of cytokines, IL-17A is known to be critical in the host defense against fungal infections; however, the function of the other IL-17 family members in anti-fungal immunity remains largely unknown. Here, we show that IL-17C expression was highly induced in kidney epithelial cells after fungal infection. Mice that lacked IL-17C exhibited increased survival and attenuated kidney tissue damage, although they had similar fungal loads. IL-17C deficiency resulted in decreased pro-inflammatory cytokine expression compared with wild-type control mice. Additionally, IL-17C directly acted on renal epithelial cells in vitro to promote pro-inflammatory cytokine production. Taken together, our data demonstrate that IL-17C is a critical factor that potentiates inflammatory responses and causes host injury during fungal infection.
