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Peripheral Autophagy and Apoptosis Elements Distinguish Sarcoidosis and Tuberculosis
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A4800 - Peripheral Autophagy and Apoptosis Elements Distinguish Sarcoidosis and Tuberculosis
Author Block: C. Schott, C. Ascoli, Y. Huang, B. Turturice, D. Perkins, P. W. Finn; Department of Medicine, University of Illinois at Chicago, Chicago, IL, United States.
Rationale: Distinguishing sarcoidosis from other granulomatous disorders, specifically tuberculosis, is challenging. Because the etiology of sarcoidosis remains unclear, studies of underlying immunological mechanisms are central to overcoming this knowledge gap. Granuloma formation in sarcoidosis and tuberculosis is regulated by IFN-γ secretion. In the periphery, pathways contributing to suppressed immune reactivity remain poorly defined, and could serve to differentiate both granulomatous disorders. To that end, we analyzed gene expression of sarcoidosis versus tuberculosis patients to identify distinct peripheral immune response features.
Methods: To analyze and compare peripheral immune response elements in sarcoidosis and tuberculosis, peripheral blood mononuclear cell expression was assessed from a publicly available microarray dataset. Using a consensus network approach, we elucidated disease-specific expression modules. From networks, gene ontology pathways were determined using DAVID (NIAID).
Results: From 10 unique modules of gene expression, 3 modules were positively associated with sarcoidosis, and 4 modules had negative associations. These modules included pathways involved in T cell activation, interferon response, and differentiation. Interestingly, 1 module was over-expressed in sarcoidosis that was under-expressed in tuberculosis. This module was centered around autophagy and apoptosis related genes FOXO3 and BCL2L1.
Conclusions: Increased autophagy and apoptosis pathways in the periphery distinguish sarcoidosis from tuberculosis. Given the unique contributions of these mechanisms to peripheral sarcoidosis responses, they provide a foundation for future study into the induction of immune reactivity in sarcoidosis.
Author Block: C. Schott, C. Ascoli, Y. Huang, B. Turturice, D. Perkins, P. W. Finn; Department of Medicine, University of Illinois at Chicago, Chicago, IL, United States.
Rationale: Distinguishing sarcoidosis from other granulomatous disorders, specifically tuberculosis, is challenging. Because the etiology of sarcoidosis remains unclear, studies of underlying immunological mechanisms are central to overcoming this knowledge gap. Granuloma formation in sarcoidosis and tuberculosis is regulated by IFN-γ secretion. In the periphery, pathways contributing to suppressed immune reactivity remain poorly defined, and could serve to differentiate both granulomatous disorders. To that end, we analyzed gene expression of sarcoidosis versus tuberculosis patients to identify distinct peripheral immune response features.
Methods: To analyze and compare peripheral immune response elements in sarcoidosis and tuberculosis, peripheral blood mononuclear cell expression was assessed from a publicly available microarray dataset. Using a consensus network approach, we elucidated disease-specific expression modules. From networks, gene ontology pathways were determined using DAVID (NIAID).
Results: From 10 unique modules of gene expression, 3 modules were positively associated with sarcoidosis, and 4 modules had negative associations. These modules included pathways involved in T cell activation, interferon response, and differentiation. Interestingly, 1 module was over-expressed in sarcoidosis that was under-expressed in tuberculosis. This module was centered around autophagy and apoptosis related genes FOXO3 and BCL2L1.
Conclusions: Increased autophagy and apoptosis pathways in the periphery distinguish sarcoidosis from tuberculosis. Given the unique contributions of these mechanisms to peripheral sarcoidosis responses, they provide a foundation for future study into the induction of immune reactivity in sarcoidosis.
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