Hypothesis: Sarcoidosis is a STAT1-mediated disease
Immunologic pathways involved in sarcoidosis pathogenesis are largely unknown. We hypothesized that patients with sarcoidosis have characteristic mRNA profiles. Microarray analysis of gene expression was done on peripheral blood (12 patients, 12 controls), lung (6 patients, 6 controls) and lymph nod...
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| Published in: | Clinical immunology (Orlando, Fla.) Vol. 132; no. 2; pp. 174 - 183 |
|---|---|
| Main Authors: | , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
| Published: |
Amsterdam
Elsevier Inc
01.08.2009
Elsevier |
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| ISSN: | 1521-6616, 1521-7035, 1521-7035 |
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| Abstract | Immunologic pathways involved in sarcoidosis pathogenesis are largely unknown. We hypothesized that patients with sarcoidosis have characteristic mRNA profiles. Microarray analysis of gene expression was done on peripheral blood (12 patients, 12 controls), lung (6 patients, 6 controls) and lymph node (8 patients, 5 controls). Comparing peripheral blood from patients with sarcoidosis to controls, 872 transcripts were upregulated and 1039 were downregulated at >
1.5-fold change and a significant
q value. Several transcripts associated with interferon and STAT1 were upregulated. Lung and lymph node analyses also showed dramatic increases in
STAT1 and
STAT1-regulated chemokines. Granulomas in lymph nodes of patients with sarcoidosis expressed abundant STAT1 and phosphorylated STAT1. STAT1 might play an important role in sarcoidosis. This novel hypothesis unites seemingly disparate observations with regard to sarcoidosis including implication of a casual role for interferons, a suspected infectious trigger, T
H1 predominating lymphocytes in bronchoalveolar lavage, and the association with hypercalcemia. |
|---|---|
| AbstractList | Immunologic pathways involved in sarcoidosis pathogenesis are largely unknown. We hypothesized that patients with sarcoidosis have characteristic mRNA profiles. Microarray analysis of gene expression was done on peripheral blood (12 patients, 12 controls), lung (6 patients, 6 controls) and lymph node (8 patients, 5 controls). Comparing peripheral blood from patients with sarcoidosis to controls, 872 transcripts were upregulated and 1039 were downregulated at >
1.5-fold change and a significant
q value. Several transcripts associated with interferon and STAT1 were upregulated. Lung and lymph node analyses also showed dramatic increases in
STAT1 and
STAT1-regulated chemokines. Granulomas in lymph nodes of patients with sarcoidosis expressed abundant STAT1 and phosphorylated STAT1. STAT1 might play an important role in sarcoidosis. This novel hypothesis unites seemingly disparate observations with regard to sarcoidosis including implication of a casual role for interferons, a suspected infectious trigger, T
H1 predominating lymphocytes in bronchoalveolar lavage, and the association with hypercalcemia. Abstract Immunologic pathways involved in sarcoidosis pathogenesis are largely unknown. We hypothesized that patients with sarcoidosis have characteristic mRNA profiles. Microarray analysis of gene expression was done on peripheral blood (12 patients, 12 controls), lung (6 patients, 6 controls) and lymph node (8 patients, 5 controls). Comparing peripheral blood from patients with sarcoidosis to controls, 872 transcripts were upregulated and 1039 were downregulated at > 1.5-fold change and a significant q value. Several transcripts associated with interferon and STAT1 were upregulated. Lung and lymph node analyses also showed dramatic increases in STAT1 and STAT1 -regulated chemokines. Granulomas in lymph nodes of patients with sarcoidosis expressed abundant STAT1 and phosphorylated STAT1. STAT1 might play an important role in sarcoidosis. This novel hypothesis unites seemingly disparate observations with regard to sarcoidosis including implication of a casual role for interferons, a suspected infectious trigger, TH 1 predominating lymphocytes in bronchoalveolar lavage, and the association with hypercalcemia. Immunologic pathways involved in sarcoidosis pathogenesis are largely unknown. We hypothesized that patients with sarcoidosis have characteristic mRNA profiles. Microarray analysis of gene expression was done on peripheral blood (12 patients, 12 controls), lung (6 patients, 6 controls) and lymph node (8 patients, 5 controls). Comparing peripheral blood from patients with sarcoidosis to controls, 872 transcripts were upregulated and 1039 were downregulated at >1.5-fold change and a significant q value. Several transcripts associated with interferon and STAT1 were upregulated. Lung and lymph node analyses also showed dramatic increases in STAT1 and STAT1-regulated chemokines. Granulomas in lymph nodes of patients with sarcoidosis expressed abundant STAT1 and phosphorylated STAT1. STAT1 might play an important role in sarcoidosis. This novel hypothesis unites seemingly disparate observations with regard to sarcoidosis including implication of a casual role for interferons, a suspected infectious trigger, T(H)1 predominating lymphocytes in bronchoalveolar lavage, and the association with hypercalcemia.Immunologic pathways involved in sarcoidosis pathogenesis are largely unknown. We hypothesized that patients with sarcoidosis have characteristic mRNA profiles. Microarray analysis of gene expression was done on peripheral blood (12 patients, 12 controls), lung (6 patients, 6 controls) and lymph node (8 patients, 5 controls). Comparing peripheral blood from patients with sarcoidosis to controls, 872 transcripts were upregulated and 1039 were downregulated at >1.5-fold change and a significant q value. Several transcripts associated with interferon and STAT1 were upregulated. Lung and lymph node analyses also showed dramatic increases in STAT1 and STAT1-regulated chemokines. Granulomas in lymph nodes of patients with sarcoidosis expressed abundant STAT1 and phosphorylated STAT1. STAT1 might play an important role in sarcoidosis. This novel hypothesis unites seemingly disparate observations with regard to sarcoidosis including implication of a casual role for interferons, a suspected infectious trigger, T(H)1 predominating lymphocytes in bronchoalveolar lavage, and the association with hypercalcemia. Immunologic pathways involved in sarcoidosis pathogenesis are largely unknown. We hypothesized that patients with sarcoidosis have characteristic mRNA profiles. Microarray analysis of gene expression was done on peripheral blood (12 patients, 12 controls), lung (6 patients, 6 controls) and lymph node (8 patients, 5 controls). Comparing peripheral blood from patients with sarcoidosis to controls, 872 transcripts were upregulated and 1039 were downregulated at >1.5-fold change and a significant q value. Several transcripts associated with interferon and STAT1 were upregulated. Lung and lymph node analyses also showed dramatic increases in STAT1 and STAT1-regulated chemokines. Granulomas in lymph nodes of patients with sarcoidosis expressed abundant STAT1 and phosphorylated STAT1. STAT1 might play an important role in sarcoidosis. This novel hypothesis unites seemingly disparate observations with regard to sarcoidosis including implication of a casual role for interferons, a suspected infectious trigger, T sub(H)1 predominating lymphocytes in bronchoalveolar lavage, and the association with hypercalcemia. Immunologic pathways involved in sarcoidosis pathogenesis are largely unknown. We hypothesized that patients with sarcoidosis have characteristic mRNA profiles. Microarray analysis of gene expression was done on peripheral blood (12 patients,12 controls), lung (6 patients, 6 controls) and lymph node (8 patients, 5 controls). Comparing peripheral blood from patients with sarcoidosis to controls, 872 transcripts were upregulated and 1039 were downregulated at ≥ 1.5-fold change and a significant q value. Several transcripts associated with interferon and STAT1 were upregulated. Lung and lymph node analyses also showed dramatic increases in STAT1 and STAT1-regulated chemokines. Granulomas in lymph nodes of patients with sarcoidosis expressed abundant STAT1 and phosphorylated STAT1. STAT1 might play an important role in sarcoidosis. This novel hypothesis unites seemingly disparate observations with regard to sarcoidosis including implication of a casual role for interferons, a suspected infectious trigger, TH1 predominating lymphocytes in bronchoalveolar lavage, and the association with hypercalcemia. Immunologic pathways involved in sarcoidosis pathogenesis are largely unknown. We hypothesized that patients with sarcoidosis have characteristic mRNA profiles. Microarray analysis of gene expression was done on peripheral blood (12 patients, 12 controls), lung (6 patients, 6 controls) and lymph node (8 patients, 5 controls). Comparing peripheral blood from patients with sarcoidosis to controls, 872 transcripts were upregulated and 1039 were downregulated at >1.5-fold change and a significant q value. Several transcripts associated with interferon and STAT1 were upregulated. Lung and lymph node analyses also showed dramatic increases in STAT1 and STAT1-regulated chemokines. Granulomas in lymph nodes of patients with sarcoidosis expressed abundant STAT1 and phosphorylated STAT1. STAT1 might play an important role in sarcoidosis. This novel hypothesis unites seemingly disparate observations with regard to sarcoidosis including implication of a casual role for interferons, a suspected infectious trigger, T(H)1 predominating lymphocytes in bronchoalveolar lavage, and the association with hypercalcemia. |
| Author | Lewis, Jinnell A. Diebel, Tessa N. Vance, Emily E. Pasadhika, Sirichai Braziel, Rita M. Choi, Dongseok Smith, Justine R. Harrington, Christina A. Rosenbaum, James T. Crouser, Elliott D. Planck, Stephen R. Austin, Carrie R. |
| AuthorAffiliation | 3 Department of Medicine, Oregon Health & Science University, Portland, OR, USA 1 Casey Eye Institute, Oregon Health & Science University, Portland, OR, USA 5 Gene Microarray Shared Resource, Oregon Health & Science University, Portland, OR, USA 7 Davis Heart & Lung Research Institute, Ohio State University Medical Center, Columbus, OH, USA 2 Department of Cell & Developmental Biology, Oregon Health & Science University, Portland, OR, USA 4 Department of Public Health & Preventive Medicine, Oregon Health & Science University, Portland, OR, USA 6 Department of Pathology, Oregon Health & Science University, Portland, OR, USA |
| AuthorAffiliation_xml | – name: 6 Department of Pathology, Oregon Health & Science University, Portland, OR, USA – name: 2 Department of Cell & Developmental Biology, Oregon Health & Science University, Portland, OR, USA – name: 4 Department of Public Health & Preventive Medicine, Oregon Health & Science University, Portland, OR, USA – name: 1 Casey Eye Institute, Oregon Health & Science University, Portland, OR, USA – name: 3 Department of Medicine, Oregon Health & Science University, Portland, OR, USA – name: 5 Gene Microarray Shared Resource, Oregon Health & Science University, Portland, OR, USA – name: 7 Davis Heart & Lung Research Institute, Ohio State University Medical Center, Columbus, OH, USA |
| Author_xml | – sequence: 1 givenname: James T. surname: Rosenbaum fullname: Rosenbaum, James T. email: rosenbaj@ohsu.edu organization: Casey Eye Institute, Oregon Health & Science University, Portland, OR, USA – sequence: 2 givenname: Sirichai surname: Pasadhika fullname: Pasadhika, Sirichai organization: Casey Eye Institute, Oregon Health & Science University, Portland, OR, USA – sequence: 3 givenname: Elliott D. surname: Crouser fullname: Crouser, Elliott D. organization: Davis Heart and Lung Research Institute, Ohio State University Medical Center, Columbus, OH, USA – sequence: 4 givenname: Dongseok surname: Choi fullname: Choi, Dongseok organization: Department of Public Health and Preventive Medicine, Oregon Health & Science University, Portland, OR, USA – sequence: 5 givenname: Christina A. surname: Harrington fullname: Harrington, Christina A. organization: Gene Microarray Shared Resource, Oregon Health & Science University, Portland, OR, USA – sequence: 6 givenname: Jinnell A. surname: Lewis fullname: Lewis, Jinnell A. organization: Casey Eye Institute, Oregon Health & Science University, Portland, OR, USA – sequence: 7 givenname: Carrie R. surname: Austin fullname: Austin, Carrie R. organization: Casey Eye Institute, Oregon Health & Science University, Portland, OR, USA – sequence: 8 givenname: Tessa N. surname: Diebel fullname: Diebel, Tessa N. organization: Casey Eye Institute, Oregon Health & Science University, Portland, OR, USA – sequence: 9 givenname: Emily E. surname: Vance fullname: Vance, Emily E. organization: Casey Eye Institute, Oregon Health & Science University, Portland, OR, USA – sequence: 10 givenname: Rita M. surname: Braziel fullname: Braziel, Rita M. organization: Oregon Health & Science University, Portland, OR, USA – sequence: 11 givenname: Justine R. surname: Smith fullname: Smith, Justine R. organization: Casey Eye Institute, Oregon Health & Science University, Portland, OR, USA – sequence: 12 givenname: Stephen R. surname: Planck fullname: Planck, Stephen R. organization: Casey Eye Institute, Oregon Health & Science University, Portland, OR, USA |
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| Keywords | Sarcoidosis Gene expression profiling Uveitis Microarray analysis Transcription factor STAT1 Eye disease Immunology Systemic disease Uvea disease Hypothesis Gene expression profile |
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| SubjectTerms | Adult Aged Allergy and Immunology Biological and medical sciences Down-Regulation Female Fundamental and applied biological sciences. Psychology Fundamental immunology Gene Expression Profiling Gene Regulatory Networks Genetic Predisposition to Disease - genetics Humans Lung - metabolism Lymph Nodes - metabolism Male Medical sciences Microarray analysis Middle Aged Models, Genetic Oligonucleotide Array Sequence Analysis - methods Ophthalmology Phosphoproteins - genetics Receptors, Interferon - genetics Sarcoidosis Sarcoidosis - genetics Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis STAT1 Transcription Factor - genetics Up-Regulation Uvea diseases Uveitis Young Adult |
| Title | Hypothesis: Sarcoidosis is a STAT1-mediated disease |
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