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Schematic illustration of the main differences between ulcerative colitis (UC, left ) and Crohn’s disease (CD, right ) in inflammation, autoinflammation and autoimmunity. The increased intestinal permeability of the epithelial cell layer allows in both diseases Danger (DAMPs) and Pathogen (PAMPs) associated molecular patterns (red dots) to easily reach the mucosa and stimulate innate immune cells. In UC neutrophil extracellular traps (NETs, green) are more abundant than in CD, activate M1 macrophages inducing TNF-α and IL-1β release. It is possible that NETs activate also the adaptive immune response causing ANCA autoantibodies production. The expression of inflammasomes, mainly NLRP1 and NLRP3, is induced in UC concurring in further enhancing IL-1β. CD4+ Th2 and CD8+ cells with IL-5, IL-13 and IFN-γ production prevails. In CD CD4+ <t>Th1</t> cells prevails over Th2 with TNF-α and IFN-γ production. M1 macrophages produce mainly IL-12, while loss of function of the inflammasomes NLRP1 and NLRP3, due to NOD2 mutations and increased Immunity-related GTPase M (IRGM) that enhances NLRP3 degradation, occurs.
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Schematic illustration of the main differences between ulcerative colitis (UC, left ) and Crohn’s disease (CD, right ) in inflammation, autoinflammation and autoimmunity. The increased intestinal permeability of the epithelial cell layer allows in both diseases Danger (DAMPs) and Pathogen (PAMPs) associated molecular patterns (red dots) to easily reach the mucosa and stimulate innate immune cells. In UC neutrophil extracellular traps (NETs, green) are more abundant than in CD, activate M1 macrophages inducing TNF-α and IL-1β release. It is possible that NETs activate also the adaptive immune response causing ANCA autoantibodies production. The expression of inflammasomes, mainly NLRP1 and NLRP3, is induced in UC concurring in further enhancing IL-1β. CD4+ Th2 and CD8+ cells with IL-5, IL-13 and IFN-γ production prevails. In CD CD4+ <t>Th1</t> cells prevails over Th2 with TNF-α and IFN-γ production. M1 macrophages produce mainly IL-12, while loss of function of the inflammasomes NLRP1 and NLRP3, due to NOD2 mutations and increased Immunity-related GTPase M (IRGM) that enhances NLRP3 degradation, occurs.
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Schematic illustration of the main differences between ulcerative colitis (UC, left ) and Crohn’s disease (CD, right ) in inflammation, autoinflammation and autoimmunity. The increased intestinal permeability of the epithelial cell layer allows in both diseases Danger (DAMPs) and Pathogen (PAMPs) associated molecular patterns (red dots) to easily reach the mucosa and stimulate innate immune cells. In UC neutrophil extracellular traps (NETs, green) are more abundant than in CD, activate M1 macrophages inducing TNF-α and IL-1β release. It is possible that NETs activate also the adaptive immune response causing ANCA autoantibodies production. The expression of inflammasomes, mainly NLRP1 and NLRP3, is induced in UC concurring in further enhancing IL-1β. CD4+ Th2 and CD8+ cells with IL-5, IL-13 and IFN-γ production prevails. In CD CD4+ <t>Th1</t> cells prevails over Th2 with TNF-α and IFN-γ production. M1 macrophages produce mainly IL-12, while loss of function of the inflammasomes NLRP1 and NLRP3, due to NOD2 mutations and increased Immunity-related GTPase M (IRGM) that enhances NLRP3 degradation, occurs.
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Schematic illustration of the main differences between ulcerative colitis (UC, left ) and Crohn’s disease (CD, right ) in inflammation, autoinflammation and autoimmunity. The increased intestinal permeability of the epithelial cell layer allows in both diseases Danger (DAMPs) and Pathogen (PAMPs) associated molecular patterns (red dots) to easily reach the mucosa and stimulate innate immune cells. In UC neutrophil extracellular traps (NETs, green) are more abundant than in CD, activate M1 macrophages inducing TNF-α and IL-1β release. It is possible that NETs activate also the adaptive immune response causing ANCA autoantibodies production. The expression of inflammasomes, mainly NLRP1 and NLRP3, is induced in UC concurring in further enhancing IL-1β. CD4+ Th2 and CD8+ cells with IL-5, IL-13 and IFN-γ production prevails. In CD CD4+ <t>Th1</t> cells prevails over Th2 with TNF-α and IFN-γ production. M1 macrophages produce mainly IL-12, while loss of function of the inflammasomes NLRP1 and NLRP3, due to NOD2 mutations and increased Immunity-related GTPase M (IRGM) that enhances NLRP3 degradation, occurs.
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Schematic illustration of the main differences between ulcerative colitis (UC, left ) and Crohn’s disease (CD, right ) in inflammation, autoinflammation and autoimmunity. The increased intestinal permeability of the epithelial cell layer allows in both diseases Danger (DAMPs) and Pathogen (PAMPs) associated molecular patterns (red dots) to easily reach the mucosa and stimulate innate immune cells. In UC neutrophil extracellular traps (NETs, green) are more abundant than in CD, activate M1 macrophages inducing TNF-α and IL-1β release. It is possible that NETs activate also the adaptive immune response causing ANCA autoantibodies production. The expression of inflammasomes, mainly NLRP1 and NLRP3, is induced in UC concurring in further enhancing IL-1β. CD4+ Th2 and CD8+ cells with IL-5, IL-13 and IFN-γ production prevails. In CD CD4+ Th1 cells prevails over Th2 with TNF-α and IFN-γ production. M1 macrophages produce mainly IL-12, while loss of function of the inflammasomes NLRP1 and NLRP3, due to NOD2 mutations and increased Immunity-related GTPase M (IRGM) that enhances NLRP3 degradation, occurs.

Journal: Current Issues in Molecular Biology

Article Title: Inflammation, Autoinflammation and Autoimmunity in Inflammatory Bowel Diseases

doi: 10.3390/cimb45070350

Figure Lengend Snippet: Schematic illustration of the main differences between ulcerative colitis (UC, left ) and Crohn’s disease (CD, right ) in inflammation, autoinflammation and autoimmunity. The increased intestinal permeability of the epithelial cell layer allows in both diseases Danger (DAMPs) and Pathogen (PAMPs) associated molecular patterns (red dots) to easily reach the mucosa and stimulate innate immune cells. In UC neutrophil extracellular traps (NETs, green) are more abundant than in CD, activate M1 macrophages inducing TNF-α and IL-1β release. It is possible that NETs activate also the adaptive immune response causing ANCA autoantibodies production. The expression of inflammasomes, mainly NLRP1 and NLRP3, is induced in UC concurring in further enhancing IL-1β. CD4+ Th2 and CD8+ cells with IL-5, IL-13 and IFN-γ production prevails. In CD CD4+ Th1 cells prevails over Th2 with TNF-α and IFN-γ production. M1 macrophages produce mainly IL-12, while loss of function of the inflammasomes NLRP1 and NLRP3, due to NOD2 mutations and increased Immunity-related GTPase M (IRGM) that enhances NLRP3 degradation, occurs.

Article Snippet: Following exposure, the intestinal mucosal immune reaction (“immunome”) leads to inflammation and tissue damage accompanied by innate and adaptive immune response, with a predominant Th1 and Th17 response with IL-12, interferon (IFN)-γ and IL-17A production in CD [ ] and a Th2 response with IL-5 and IL-13 production in UC ( ) [ , ].

Techniques: Permeability, Expressing

Cytokines with a major role in IBD. Data reported in this table were obtained from [ <xref ref-type= 47 , 58 , 85 , 96 ]." width="100%" height="100%">

Journal: Current Issues in Molecular Biology

Article Title: Inflammation, Autoinflammation and Autoimmunity in Inflammatory Bowel Diseases

doi: 10.3390/cimb45070350

Figure Lengend Snippet: Cytokines with a major role in IBD. Data reported in this table were obtained from [ 47 , 58 , 85 , 96 ].

Article Snippet: Following exposure, the intestinal mucosal immune reaction (“immunome”) leads to inflammation and tissue damage accompanied by innate and adaptive immune response, with a predominant Th1 and Th17 response with IL-12, interferon (IFN)-γ and IL-17A production in CD [ ] and a Th2 response with IL-5 and IL-13 production in UC ( ) [ , ].

Techniques: Activation Assay, Immunopeptidomics, Cell Differentiation, Blocking Assay