Membranous Glomerulonephritis Development with Th2-Type Immune Deviations in MRL/lpr Mice Deficient for IL-27 Receptor (WSX-1)
MRL/lpr mice develop spontaneous glomerulonephritis that is essentially identical with diffuse proliferative glomerulonephritis (World Health Organization class IV) in human lupus nephritis. Lupus nephritis is one of the most serious complications of systemic lupus erythematosus. Diffuse proliferati...
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| Veröffentlicht in: | Journal of Immunology 2005-12, Vol.175 (11), p.7185-7192 |
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| creator | Shimizu, Sakiko Sugiyama, Naonobu Masutani, Kohsuke Sadanaga, Atsushi Miyazaki, Yoshiyuki Inoue, Yasushi Akahoshi, Mitsuteru Katafuchi, Ritsuko Hirakata, Hideki Harada, Mine Hamano, Shinjiro Nakashima, Hitoshi Yoshida, Hiroki |
| description | MRL/lpr mice develop spontaneous glomerulonephritis that is essentially identical with diffuse proliferative glomerulonephritis (World Health Organization class IV) in human lupus nephritis. Lupus nephritis is one of the most serious complications of systemic lupus erythematosus. Diffuse proliferative glomerulonephritis is associated with autoimmune responses dominated by Th1 cells producing high levels of IFN-gamma. The initial mounting of Th1 responses depends on the function of the WSX-1 gene, which encodes a subunit of the IL-27R with homology to IL-12R. In mice deficient for the WSX-1 gene, proper Th1 differentiation was impaired and abnormal Th2 skewing was observed during infection with some intracellular pathogens. Disruption of the WSX-1 gene dramatically changed the pathophysiology of glomerulonephritis developing in MRL/lpr mice. WSX-1-/- MRL/lpr mice developed disease resembling human membranous glomerulonephritis (World Health Organization class V) with a predominance of IgG1 in glomerular deposits, accompanied by increased IgG1 and IgE in the sera. T cells in WSX-1-/- MRL/lpr mice displayed significantly reduced IFN-gamma production along with elevated IL-4 expression. Loss of WSX-1 thus favors Th2-type autoimmune responses, suggesting that the Th1/Th2 balance may be a pivotal determinant of human lupus nephritis development. |
| doi_str_mv | 10.4049/jimmunol.175.11.7185 |
| format | Article |
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Lupus nephritis is one of the most serious complications of systemic lupus erythematosus. Diffuse proliferative glomerulonephritis is associated with autoimmune responses dominated by Th1 cells producing high levels of IFN-gamma. The initial mounting of Th1 responses depends on the function of the WSX-1 gene, which encodes a subunit of the IL-27R with homology to IL-12R. In mice deficient for the WSX-1 gene, proper Th1 differentiation was impaired and abnormal Th2 skewing was observed during infection with some intracellular pathogens. Disruption of the WSX-1 gene dramatically changed the pathophysiology of glomerulonephritis developing in MRL/lpr mice. WSX-1-/- MRL/lpr mice developed disease resembling human membranous glomerulonephritis (World Health Organization class V) with a predominance of IgG1 in glomerular deposits, accompanied by increased IgG1 and IgE in the sera. T cells in WSX-1-/- MRL/lpr mice displayed significantly reduced IFN-gamma production along with elevated IL-4 expression. Loss of WSX-1 thus favors Th2-type autoimmune responses, suggesting that the Th1/Th2 balance may be a pivotal determinant of human lupus nephritis development.</description><identifier>ISSN: 0022-1767</identifier><identifier>EISSN: 1550-6606</identifier><identifier>EISSN: 1365-2567</identifier><identifier>DOI: 10.4049/jimmunol.175.11.7185</identifier><identifier>PMID: 16301622</identifier><language>eng</language><publisher>United States: Am Assoc Immnol</publisher><subject>Animals ; Disease Models, Animal ; Enzyme-Linked Immunosorbent Assay ; Female ; Glomerulonephritis, Membranous - genetics ; Glomerulonephritis, Membranous - immunology ; Glomerulonephritis, Membranous - pathology ; Immunoglobulin E - analysis ; Immunoglobulin G - analysis ; Immunohistochemistry ; Interferon-gamma - immunology ; Interleukin-4 - immunology ; Lupus Nephritis - genetics ; Lupus Nephritis - immunology ; Lupus Nephritis - pathology ; Mice ; Mice, Inbred MRL lpr - genetics ; Mice, Inbred MRL lpr - immunology ; Mice, Mutant Strains ; Microscopy, Electron, Transmission ; Receptors, Cytokine - deficiency ; Receptors, Cytokine - genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Th1 Cells - immunology ; Th2 Cells - immunology</subject><ispartof>Journal of Immunology, 2005-12, Vol.175 (11), p.7185-7192</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c415t-3164026b1c960008392f52a141e3a77799d129a685b31f6a378d26110643c9cc3</citedby><cites>FETCH-LOGICAL-c415t-3164026b1c960008392f52a141e3a77799d129a685b31f6a378d26110643c9cc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16301622$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shimizu, Sakiko</creatorcontrib><creatorcontrib>Sugiyama, Naonobu</creatorcontrib><creatorcontrib>Masutani, Kohsuke</creatorcontrib><creatorcontrib>Sadanaga, Atsushi</creatorcontrib><creatorcontrib>Miyazaki, Yoshiyuki</creatorcontrib><creatorcontrib>Inoue, Yasushi</creatorcontrib><creatorcontrib>Akahoshi, Mitsuteru</creatorcontrib><creatorcontrib>Katafuchi, Ritsuko</creatorcontrib><creatorcontrib>Hirakata, Hideki</creatorcontrib><creatorcontrib>Harada, Mine</creatorcontrib><creatorcontrib>Hamano, Shinjiro</creatorcontrib><creatorcontrib>Nakashima, Hitoshi</creatorcontrib><creatorcontrib>Yoshida, Hiroki</creatorcontrib><title>Membranous Glomerulonephritis Development with Th2-Type Immune Deviations in MRL/lpr Mice Deficient for IL-27 Receptor (WSX-1)</title><title>Journal of Immunology</title><addtitle>J Immunol</addtitle><description>MRL/lpr mice develop spontaneous glomerulonephritis that is essentially identical with diffuse proliferative glomerulonephritis (World Health Organization class IV) in human lupus nephritis. Lupus nephritis is one of the most serious complications of systemic lupus erythematosus. Diffuse proliferative glomerulonephritis is associated with autoimmune responses dominated by Th1 cells producing high levels of IFN-gamma. The initial mounting of Th1 responses depends on the function of the WSX-1 gene, which encodes a subunit of the IL-27R with homology to IL-12R. In mice deficient for the WSX-1 gene, proper Th1 differentiation was impaired and abnormal Th2 skewing was observed during infection with some intracellular pathogens. Disruption of the WSX-1 gene dramatically changed the pathophysiology of glomerulonephritis developing in MRL/lpr mice. WSX-1-/- MRL/lpr mice developed disease resembling human membranous glomerulonephritis (World Health Organization class V) with a predominance of IgG1 in glomerular deposits, accompanied by increased IgG1 and IgE in the sera. T cells in WSX-1-/- MRL/lpr mice displayed significantly reduced IFN-gamma production along with elevated IL-4 expression. Loss of WSX-1 thus favors Th2-type autoimmune responses, suggesting that the Th1/Th2 balance may be a pivotal determinant of human lupus nephritis development.</description><subject>Animals</subject><subject>Disease Models, Animal</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Female</subject><subject>Glomerulonephritis, Membranous - genetics</subject><subject>Glomerulonephritis, Membranous - immunology</subject><subject>Glomerulonephritis, Membranous - pathology</subject><subject>Immunoglobulin E - analysis</subject><subject>Immunoglobulin G - analysis</subject><subject>Immunohistochemistry</subject><subject>Interferon-gamma - immunology</subject><subject>Interleukin-4 - immunology</subject><subject>Lupus Nephritis - genetics</subject><subject>Lupus Nephritis - immunology</subject><subject>Lupus Nephritis - pathology</subject><subject>Mice</subject><subject>Mice, Inbred MRL lpr - genetics</subject><subject>Mice, Inbred MRL lpr - immunology</subject><subject>Mice, Mutant Strains</subject><subject>Microscopy, Electron, Transmission</subject><subject>Receptors, Cytokine - deficiency</subject><subject>Receptors, Cytokine - genetics</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Th1 Cells - immunology</subject><subject>Th2 Cells - immunology</subject><issn>0022-1767</issn><issn>1550-6606</issn><issn>1365-2567</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc2KFDEUhYMoTjv6BiJZybiontz8VpYy6tjQjTC26C6k0ykrQ-rHpMpiNj67VXSL7lyFS75zLpcPoZdA1pxwfX0fmmZsu7gGJdYAawWleIRWIAQppCTyMVoRQmkBSqoL9Czne0KIJJQ_RRcgGQFJ6Qr92vnmkGzbjRnfxq7xaYxd6_s6hSFk_M7_9LHrG98OeApDjfc1LfYPvcebZbtfgGCH0LUZhxbv7rbXsU94F9zyVQUXlmTVJbzZFlThO-98P8zj1dfP3wp48xw9qWzM_sX5vURfPrzf33wstp9uNzdvt4XjIIaCgeSEygM4LecrSqZpJagFDp5ZpZTWR6DaylIcGFTSMlUeqQQgkjOnnWOX6PWpt0_dj9HnwTQhOx-jbf18upFlCYIr_V8QNCup4HQG-Ql0qcs5-cr0KTQ2PRggZhFk_ggysyADYBZBc-zVuX88NP74N3Q2MgNXJ6AO3-spJG9yY2OccTDTNP3b9RvII5oc</recordid><startdate>20051201</startdate><enddate>20051201</enddate><creator>Shimizu, Sakiko</creator><creator>Sugiyama, Naonobu</creator><creator>Masutani, Kohsuke</creator><creator>Sadanaga, Atsushi</creator><creator>Miyazaki, Yoshiyuki</creator><creator>Inoue, Yasushi</creator><creator>Akahoshi, Mitsuteru</creator><creator>Katafuchi, Ritsuko</creator><creator>Hirakata, Hideki</creator><creator>Harada, Mine</creator><creator>Hamano, Shinjiro</creator><creator>Nakashima, Hitoshi</creator><creator>Yoshida, Hiroki</creator><general>Am Assoc Immnol</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20051201</creationdate><title>Membranous Glomerulonephritis Development with Th2-Type Immune Deviations in MRL/lpr Mice Deficient for IL-27 Receptor (WSX-1)</title><author>Shimizu, Sakiko ; Sugiyama, Naonobu ; Masutani, Kohsuke ; Sadanaga, Atsushi ; Miyazaki, Yoshiyuki ; Inoue, Yasushi ; Akahoshi, Mitsuteru ; Katafuchi, Ritsuko ; Hirakata, Hideki ; Harada, Mine ; Hamano, Shinjiro ; Nakashima, Hitoshi ; Yoshida, Hiroki</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c415t-3164026b1c960008392f52a141e3a77799d129a685b31f6a378d26110643c9cc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Disease Models, Animal</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Female</topic><topic>Glomerulonephritis, Membranous - genetics</topic><topic>Glomerulonephritis, Membranous - immunology</topic><topic>Glomerulonephritis, Membranous - pathology</topic><topic>Immunoglobulin E - analysis</topic><topic>Immunoglobulin G - analysis</topic><topic>Immunohistochemistry</topic><topic>Interferon-gamma - immunology</topic><topic>Interleukin-4 - immunology</topic><topic>Lupus Nephritis - genetics</topic><topic>Lupus Nephritis - immunology</topic><topic>Lupus Nephritis - pathology</topic><topic>Mice</topic><topic>Mice, Inbred MRL lpr - genetics</topic><topic>Mice, Inbred MRL lpr - immunology</topic><topic>Mice, Mutant Strains</topic><topic>Microscopy, Electron, Transmission</topic><topic>Receptors, Cytokine - deficiency</topic><topic>Receptors, Cytokine - genetics</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Th1 Cells - immunology</topic><topic>Th2 Cells - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shimizu, Sakiko</creatorcontrib><creatorcontrib>Sugiyama, Naonobu</creatorcontrib><creatorcontrib>Masutani, Kohsuke</creatorcontrib><creatorcontrib>Sadanaga, Atsushi</creatorcontrib><creatorcontrib>Miyazaki, Yoshiyuki</creatorcontrib><creatorcontrib>Inoue, Yasushi</creatorcontrib><creatorcontrib>Akahoshi, Mitsuteru</creatorcontrib><creatorcontrib>Katafuchi, Ritsuko</creatorcontrib><creatorcontrib>Hirakata, Hideki</creatorcontrib><creatorcontrib>Harada, Mine</creatorcontrib><creatorcontrib>Hamano, Shinjiro</creatorcontrib><creatorcontrib>Nakashima, Hitoshi</creatorcontrib><creatorcontrib>Yoshida, Hiroki</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of Immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shimizu, Sakiko</au><au>Sugiyama, Naonobu</au><au>Masutani, Kohsuke</au><au>Sadanaga, Atsushi</au><au>Miyazaki, Yoshiyuki</au><au>Inoue, Yasushi</au><au>Akahoshi, Mitsuteru</au><au>Katafuchi, Ritsuko</au><au>Hirakata, Hideki</au><au>Harada, Mine</au><au>Hamano, Shinjiro</au><au>Nakashima, Hitoshi</au><au>Yoshida, Hiroki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Membranous Glomerulonephritis Development with Th2-Type Immune Deviations in MRL/lpr Mice Deficient for IL-27 Receptor (WSX-1)</atitle><jtitle>Journal of Immunology</jtitle><addtitle>J Immunol</addtitle><date>2005-12-01</date><risdate>2005</risdate><volume>175</volume><issue>11</issue><spage>7185</spage><epage>7192</epage><pages>7185-7192</pages><issn>0022-1767</issn><eissn>1550-6606</eissn><eissn>1365-2567</eissn><abstract>MRL/lpr mice develop spontaneous glomerulonephritis that is essentially identical with diffuse proliferative glomerulonephritis (World Health Organization class IV) in human lupus nephritis. Lupus nephritis is one of the most serious complications of systemic lupus erythematosus. Diffuse proliferative glomerulonephritis is associated with autoimmune responses dominated by Th1 cells producing high levels of IFN-gamma. The initial mounting of Th1 responses depends on the function of the WSX-1 gene, which encodes a subunit of the IL-27R with homology to IL-12R. In mice deficient for the WSX-1 gene, proper Th1 differentiation was impaired and abnormal Th2 skewing was observed during infection with some intracellular pathogens. Disruption of the WSX-1 gene dramatically changed the pathophysiology of glomerulonephritis developing in MRL/lpr mice. WSX-1-/- MRL/lpr mice developed disease resembling human membranous glomerulonephritis (World Health Organization class V) with a predominance of IgG1 in glomerular deposits, accompanied by increased IgG1 and IgE in the sera. T cells in WSX-1-/- MRL/lpr mice displayed significantly reduced IFN-gamma production along with elevated IL-4 expression. Loss of WSX-1 thus favors Th2-type autoimmune responses, suggesting that the Th1/Th2 balance may be a pivotal determinant of human lupus nephritis development.</abstract><cop>United States</cop><pub>Am Assoc Immnol</pub><pmid>16301622</pmid><doi>10.4049/jimmunol.175.11.7185</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Journal of Immunology, 2005-12, Vol.175 (11), p.7185-7192 |
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| subjects | Animals Disease Models, Animal Enzyme-Linked Immunosorbent Assay Female Glomerulonephritis, Membranous - genetics Glomerulonephritis, Membranous - immunology Glomerulonephritis, Membranous - pathology Immunoglobulin E - analysis Immunoglobulin G - analysis Immunohistochemistry Interferon-gamma - immunology Interleukin-4 - immunology Lupus Nephritis - genetics Lupus Nephritis - immunology Lupus Nephritis - pathology Mice Mice, Inbred MRL lpr - genetics Mice, Inbred MRL lpr - immunology Mice, Mutant Strains Microscopy, Electron, Transmission Receptors, Cytokine - deficiency Receptors, Cytokine - genetics Reverse Transcriptase Polymerase Chain Reaction Th1 Cells - immunology Th2 Cells - immunology |
| title | Membranous Glomerulonephritis Development with Th2-Type Immune Deviations in MRL/lpr Mice Deficient for IL-27 Receptor (WSX-1) |
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