The ARTS 1 gene is also known as the ERAP 1 gene: http://www.ncbi.nlm.nih.gov/sites/entre ... uids=51752
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http://parsplanitisforum.yuku.com/topic/28
here are some newly discovered genetic links to Ankylosing spondlyitis and other autoimmune disease processes
recently the ANTXR2 and IL1R2 genes were discovered and the association with IL23R and ERAP1 (formerly ARTS!) genes were confirmed so in addition to HLA B27 the following genes are linked in anglo american and european persons:
HLA B27
ANTXR2
IL1R2
IL23R
ERAP1 (formerly ARTS1)
http://www.medscape.com/viewarticle/564590
"The diseases linked to these genes are ankylosing spondylitis (AS), autoimmune thyroid disease (AITD), multiple sclerosis, and breast cancer.
The investigators suggest that IL23R, in particular, may be a common susceptibility factor for the major "seronegative" diseases. Earlier research has shown an association between IL23R and both inflammatory bowel disease (Crohn's disease) and psoriasis. "
http://www.medscape.com/viewarticle/566849?src=mp
research article
Ankylosing Spondylitis, Crohn's disease, Systemic Lupus Erythematosis, Multiple Sclerosis
http://www.medscape.com/viewarticle/564590
expanded search on IL23 in Uvieitis shows increase in this cytokine in Behcet's patients,VKH patients etc
http://www.google.com/search?hl=en&q=IL ... h&aq=f&oq=
patent for anti IL23 in uveitis:
http://www.freshpatents.com/Use-of-il-2 ... 199460.php
research (with mice) and patent information
http://www.wipo.int/pctdb/en/wo.jsp?IA= ... SPLAY=DESC
simvastatin used to treat cholesterol levels inhibits IL17
http://www.jimmunol.org/cgi/content/abs ... 80/10/6988
IL23R, ERAP1. IL23R, ANTXR2, IL1R2, 4 major disorders
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IL23R, ERAP1. IL23R, ANTXR2, IL1R2, 4 major disorders
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Re: IL23R, ARTS1 genes and 4 major disorders
http://www.ncbi.nlm.nih.gov/pubmed/1844 ... t=Abstract
a series of abstracts on research into various autoimmune disease processes to include Ankylosing Spondylitis, Rheumatoid arthritis, Systemic Lupus Erythematosus, Sjogren's syndrome, Crohn's disease and various cytokines, chemokines, gentics and disease modification with DMARD and Biological Response modifying drugs
IL23R in celiac disease and Multiple sclerosis (subset genes Identified for susceptibility for MS)
http://www.ncbi.nlm.nih.gov/sites/entre ... h=18368064
a series of abstracts on research into various autoimmune disease processes to include Ankylosing Spondylitis, Rheumatoid arthritis, Systemic Lupus Erythematosus, Sjogren's syndrome, Crohn's disease and various cytokines, chemokines, gentics and disease modification with DMARD and Biological Response modifying drugs
IL23R in celiac disease and Multiple sclerosis (subset genes Identified for susceptibility for MS)
http://www.ncbi.nlm.nih.gov/sites/entre ... h=18368064
Mike Bartolatz
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Re: IL23R, ARTS1 genes and 4 major disorders
IL23 R in a white Spanish population with specific subset for Multiple Sclerosis.
http://www.ncbi.nlm.nih.gov/sites/entre ... h=18368064
http://www.ncbi.nlm.nih.gov/sites/entre ... h=18368064
Mike Bartolatz
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Re: IL23R, ARTS1 genes and 4 major disorders
TH17
1: Immunol Res. 2008;41(2):87-102. Links
Th17 cells: a new fate for differentiating helper T cells.Chen Z, O'Shea JJ.
Molecular Immunology and Inflammation Branch, National Institutes of Arthritis, Musculoskeletal and Skin Diseases, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA. zchen@utu.fi
Classically naïve CD4(+) have been thought to differentiate into two possible lineages, T helper 1 (Th1) or T helper 2 (Th2) cells. Within this paradigm the pathogenesis of autoimmunity was suggested to predominantly relate to Th1 cells and the production of IFN-gamma. However, there were many aspects of this model that did not seem to fit, not the least of which was that IFN-gamma was protective in some models of autoimmunity. During the past 2 years, remarkable progress has been made to characterize a new lineage of helper T cells. Designated Th17 cells, this lineage selectively produces proinflammatory cytokines including IL-17, IL-21, and IL-22. In the mouse, the differentiation of this new lineage is initiated by TGFbeta-1 and IL-6 and IL-21, which activate Stat3 and induce the expression of the transcription factor retinoic acid-related orphan receptor (RORgammat). IL-23, which also activates Stat3, apparently serves to maintain Th17 cells in vivo. In human cells, IL-1, IL-6, and IL-23 promote human Th17 differentiation, but TGFbeta-1 is reportedly not needed. Emerging data have suggested that Th17 plays an essential role in the host defense against extracellular bacteria and fungi and in pathogenesis of autoimmune diseases. Selectively targeting the Th17 lineage may be beneficial for the treatment of inflammatory and autoimmune diseases.
PMID: 18172584 [PubMed - indexed for MEDLINE]
1: Immunol Res. 2008;41(2):87-102. Links
Th17 cells: a new fate for differentiating helper T cells.Chen Z, O'Shea JJ.
Molecular Immunology and Inflammation Branch, National Institutes of Arthritis, Musculoskeletal and Skin Diseases, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA. zchen@utu.fi
Classically naïve CD4(+) have been thought to differentiate into two possible lineages, T helper 1 (Th1) or T helper 2 (Th2) cells. Within this paradigm the pathogenesis of autoimmunity was suggested to predominantly relate to Th1 cells and the production of IFN-gamma. However, there were many aspects of this model that did not seem to fit, not the least of which was that IFN-gamma was protective in some models of autoimmunity. During the past 2 years, remarkable progress has been made to characterize a new lineage of helper T cells. Designated Th17 cells, this lineage selectively produces proinflammatory cytokines including IL-17, IL-21, and IL-22. In the mouse, the differentiation of this new lineage is initiated by TGFbeta-1 and IL-6 and IL-21, which activate Stat3 and induce the expression of the transcription factor retinoic acid-related orphan receptor (RORgammat). IL-23, which also activates Stat3, apparently serves to maintain Th17 cells in vivo. In human cells, IL-1, IL-6, and IL-23 promote human Th17 differentiation, but TGFbeta-1 is reportedly not needed. Emerging data have suggested that Th17 plays an essential role in the host defense against extracellular bacteria and fungi and in pathogenesis of autoimmune diseases. Selectively targeting the Th17 lineage may be beneficial for the treatment of inflammatory and autoimmune diseases.
PMID: 18172584 [PubMed - indexed for MEDLINE]
Mike Bartolatz
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Re: IL23R, ARTS1 genes and 4 major disorders
http://www.ncbi.nlm.nih.gov/pubmed/1934 ... rom=pubmed
Calcitriol suppresses experimental autoimmune uveitis (in mice)
Calcitriol suppresses experimental autoimmune uveitis (in mice)
Mike Bartolatz
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