Prevention of Collagen-Induced Arthritis in Mice Transgenic for the Complement Inhibitor Complement Receptor 1-Related Gene/Protein y
The objective of these studies was to examine collagen-induced arthritis (CIA) in C57BL/6 mice transgenic for the rodent complement regulatory protein complement receptor 1-related gene/protein y (Crry) (Crry-Tg), a C3 convertase inhibitor. The scores for clinical disease activity and for histologic...
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description | The objective of these studies was to examine collagen-induced arthritis (CIA) in C57BL/6 mice transgenic for the rodent complement regulatory protein complement receptor 1-related gene/protein y (Crry) (Crry-Tg), a C3 convertase inhibitor. The scores for clinical disease activity and for histological damage in the joints were both significantly decreased in Crry-Tg mice in comparison to wild-type (WT) littermates. The production of both IgG1 and IgG2a anti-collagen Abs was reduced in the Crry-Tg mice, although spleen cell proliferation in response to collagen type II was not altered. The production of IFN-gamma, TNF-alpha, and IL-1beta by LPS-stimulated spleen cells was decreased, and IL-10 was increased, in cells from Crry-Tg mice in comparison to WT. The steady-state mRNA levels for IFN-gamma, TNF-alpha, and IL-1beta were all decreased in the joints of Crry-Tg mice in comparison to WT. The synovium from Crry-Tg mice without CIA contained the mRNA for the Crry transgene, by RT-PCR, and the synovium from transgenic mice with CIA exhibited little deposition of C3 protein by immunohistological analysis. These results suggest that suppression of CIA in Crry-Tg mice may be due to enhanced synthesis of Crry locally in the joint with decreased production of proinflammatory cytokines. |
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Michael ; Arend, William P</creator><creatorcontrib>Banda, Nirmal K ; Kraus, Damian M ; Muggli, Michele ; Bendele, Alison ; Holers, V. Michael ; Arend, William P</creatorcontrib><description>The objective of these studies was to examine collagen-induced arthritis (CIA) in C57BL/6 mice transgenic for the rodent complement regulatory protein complement receptor 1-related gene/protein y (Crry) (Crry-Tg), a C3 convertase inhibitor. The scores for clinical disease activity and for histological damage in the joints were both significantly decreased in Crry-Tg mice in comparison to wild-type (WT) littermates. The production of both IgG1 and IgG2a anti-collagen Abs was reduced in the Crry-Tg mice, although spleen cell proliferation in response to collagen type II was not altered. The production of IFN-gamma, TNF-alpha, and IL-1beta by LPS-stimulated spleen cells was decreased, and IL-10 was increased, in cells from Crry-Tg mice in comparison to WT. The steady-state mRNA levels for IFN-gamma, TNF-alpha, and IL-1beta were all decreased in the joints of Crry-Tg mice in comparison to WT. The synovium from Crry-Tg mice without CIA contained the mRNA for the Crry transgene, by RT-PCR, and the synovium from transgenic mice with CIA exhibited little deposition of C3 protein by immunohistological analysis. These results suggest that suppression of CIA in Crry-Tg mice may be due to enhanced synthesis of Crry locally in the joint with decreased production of proinflammatory cytokines.</description><identifier>ISSN: 0022-1767</identifier><identifier>EISSN: 1550-6606</identifier><identifier>DOI: 10.4049/jimmunol.171.4.2109</identifier><identifier>PMID: 12902517</identifier><language>eng</language><publisher>United States: Am Assoc Immnol</publisher><subject>Animals ; Arthritis, Experimental - genetics ; Arthritis, Experimental - immunology ; Arthritis, Experimental - pathology ; Arthritis, Experimental - prevention & control ; Autoantibodies - biosynthesis ; Autoantibodies - blood ; Cattle ; Collagen Type II - administration & dosage ; Collagen Type II - immunology ; Complement Inactivator Proteins - genetics ; Cytokines - biosynthesis ; Female ; Hindlimb ; Immunoglobulin G - biosynthesis ; Immunoglobulin G - blood ; Immunohistochemistry ; Injections, Intradermal ; Lymph Nodes - cytology ; Lymph Nodes - immunology ; Lymphocyte Activation - genetics ; Lymphocyte Subsets - immunology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Receptors, Complement - biosynthesis ; Receptors, Complement - genetics ; Receptors, Complement 3b - genetics ; RNA, Messenger - analysis ; Spleen - cytology ; Spleen - immunology ; Spleen - metabolism</subject><ispartof>The Journal of immunology (1950), 2003-08, Vol.171 (4), p.2109-2115</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c475t-b48820346cb5870992a82faeae5951bbfece5e804550d4d713188fad346a228e3</citedby><cites>FETCH-LOGICAL-c475t-b48820346cb5870992a82faeae5951bbfece5e804550d4d713188fad346a228e3</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/12902517$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Banda, Nirmal K</creatorcontrib><creatorcontrib>Kraus, Damian M</creatorcontrib><creatorcontrib>Muggli, Michele</creatorcontrib><creatorcontrib>Bendele, Alison</creatorcontrib><creatorcontrib>Holers, V. Michael</creatorcontrib><creatorcontrib>Arend, William P</creatorcontrib><title>Prevention of Collagen-Induced Arthritis in Mice Transgenic for the Complement Inhibitor Complement Receptor 1-Related Gene/Protein y</title><title>The Journal of immunology (1950)</title><addtitle>J Immunol</addtitle><description>The objective of these studies was to examine collagen-induced arthritis (CIA) in C57BL/6 mice transgenic for the rodent complement regulatory protein complement receptor 1-related gene/protein y (Crry) (Crry-Tg), a C3 convertase inhibitor. The scores for clinical disease activity and for histological damage in the joints were both significantly decreased in Crry-Tg mice in comparison to wild-type (WT) littermates. The production of both IgG1 and IgG2a anti-collagen Abs was reduced in the Crry-Tg mice, although spleen cell proliferation in response to collagen type II was not altered. The production of IFN-gamma, TNF-alpha, and IL-1beta by LPS-stimulated spleen cells was decreased, and IL-10 was increased, in cells from Crry-Tg mice in comparison to WT. The steady-state mRNA levels for IFN-gamma, TNF-alpha, and IL-1beta were all decreased in the joints of Crry-Tg mice in comparison to WT. The synovium from Crry-Tg mice without CIA contained the mRNA for the Crry transgene, by RT-PCR, and the synovium from transgenic mice with CIA exhibited little deposition of C3 protein by immunohistological analysis. These results suggest that suppression of CIA in Crry-Tg mice may be due to enhanced synthesis of Crry locally in the joint with decreased production of proinflammatory cytokines.</description><subject>Animals</subject><subject>Arthritis, Experimental - genetics</subject><subject>Arthritis, Experimental - immunology</subject><subject>Arthritis, Experimental - pathology</subject><subject>Arthritis, Experimental - prevention & control</subject><subject>Autoantibodies - biosynthesis</subject><subject>Autoantibodies - blood</subject><subject>Cattle</subject><subject>Collagen Type II - administration & dosage</subject><subject>Collagen Type II - immunology</subject><subject>Complement Inactivator Proteins - genetics</subject><subject>Cytokines - biosynthesis</subject><subject>Female</subject><subject>Hindlimb</subject><subject>Immunoglobulin G - biosynthesis</subject><subject>Immunoglobulin G - blood</subject><subject>Immunohistochemistry</subject><subject>Injections, Intradermal</subject><subject>Lymph Nodes - cytology</subject><subject>Lymph Nodes - immunology</subject><subject>Lymphocyte Activation - genetics</subject><subject>Lymphocyte Subsets - immunology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Transgenic</subject><subject>Receptors, Complement - biosynthesis</subject><subject>Receptors, Complement - genetics</subject><subject>Receptors, Complement 3b - genetics</subject><subject>RNA, Messenger - analysis</subject><subject>Spleen - cytology</subject><subject>Spleen - immunology</subject><subject>Spleen - metabolism</subject><issn>0022-1767</issn><issn>1550-6606</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1q3DAURkVpaSZpn6AQtGpXnkiy5J9lGNJkIKEhpGsh29exgi1NJDnDPEDfu3eYKc0uK8HV-Y7Q_Qj5xtlSMllfPNtpmp0fl7zkS7kUnNUfyIIrxbKiYMVHsmBMiIyXRXlCTmN8ZowVTMjP5ISLmgnFywX5cx_gFVyy3lHf05UfR_MELlu7bm6ho5chDcEmG6l19M62QB-DcRER29LeB5oGwNS0GWFCDV27wTY24cWb4QO0sNnPePYAo0novQYHF_fBJ0Dv7gv51JsxwtfjeUZ-_7x6XN1kt7-u16vL26yVpUpZI6tKsFwWbaOqktW1MJXoDRhQteJN0-M7CiomcQed7Eqe86rqTYcJI0QF-Rn5fvBugn-ZISY92dgC_tmBn6MucyVwd-pdEL34Cs8RzA9gG3yMAXq9CXYyYac50_ua9L-aNNakpd7XhKnzo35uJuj-Z469IPDjAAz2adjaADpOZhwR53q73b5R_QWSLJ88</recordid><startdate>20030815</startdate><enddate>20030815</enddate><creator>Banda, Nirmal K</creator><creator>Kraus, Damian M</creator><creator>Muggli, Michele</creator><creator>Bendele, Alison</creator><creator>Holers, V. Michael</creator><creator>Arend, William P</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>20030815</creationdate><title>Prevention of Collagen-Induced Arthritis in Mice Transgenic for the Complement Inhibitor Complement Receptor 1-Related Gene/Protein y</title><author>Banda, Nirmal K ; Kraus, Damian M ; Muggli, Michele ; Bendele, Alison ; Holers, V. Michael ; Arend, William P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c475t-b48820346cb5870992a82faeae5951bbfece5e804550d4d713188fad346a228e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Arthritis, Experimental - genetics</topic><topic>Arthritis, Experimental - immunology</topic><topic>Arthritis, Experimental - pathology</topic><topic>Arthritis, Experimental - prevention & control</topic><topic>Autoantibodies - biosynthesis</topic><topic>Autoantibodies - blood</topic><topic>Cattle</topic><topic>Collagen Type II - administration & dosage</topic><topic>Collagen Type II - immunology</topic><topic>Complement Inactivator Proteins - genetics</topic><topic>Cytokines - biosynthesis</topic><topic>Female</topic><topic>Hindlimb</topic><topic>Immunoglobulin G - biosynthesis</topic><topic>Immunoglobulin G - blood</topic><topic>Immunohistochemistry</topic><topic>Injections, Intradermal</topic><topic>Lymph Nodes - cytology</topic><topic>Lymph Nodes - immunology</topic><topic>Lymphocyte Activation - genetics</topic><topic>Lymphocyte Subsets - immunology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Transgenic</topic><topic>Receptors, Complement - biosynthesis</topic><topic>Receptors, Complement - genetics</topic><topic>Receptors, Complement 3b - genetics</topic><topic>RNA, Messenger - analysis</topic><topic>Spleen - cytology</topic><topic>Spleen - immunology</topic><topic>Spleen - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Banda, Nirmal K</creatorcontrib><creatorcontrib>Kraus, Damian M</creatorcontrib><creatorcontrib>Muggli, Michele</creatorcontrib><creatorcontrib>Bendele, Alison</creatorcontrib><creatorcontrib>Holers, V. Michael</creatorcontrib><creatorcontrib>Arend, William P</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>The Journal of immunology (1950)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Banda, Nirmal K</au><au>Kraus, Damian M</au><au>Muggli, Michele</au><au>Bendele, Alison</au><au>Holers, V. Michael</au><au>Arend, William P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Prevention of Collagen-Induced Arthritis in Mice Transgenic for the Complement Inhibitor Complement Receptor 1-Related Gene/Protein y</atitle><jtitle>The Journal of immunology (1950)</jtitle><addtitle>J Immunol</addtitle><date>2003-08-15</date><risdate>2003</risdate><volume>171</volume><issue>4</issue><spage>2109</spage><epage>2115</epage><pages>2109-2115</pages><issn>0022-1767</issn><eissn>1550-6606</eissn><abstract>The objective of these studies was to examine collagen-induced arthritis (CIA) in C57BL/6 mice transgenic for the rodent complement regulatory protein complement receptor 1-related gene/protein y (Crry) (Crry-Tg), a C3 convertase inhibitor. The scores for clinical disease activity and for histological damage in the joints were both significantly decreased in Crry-Tg mice in comparison to wild-type (WT) littermates. The production of both IgG1 and IgG2a anti-collagen Abs was reduced in the Crry-Tg mice, although spleen cell proliferation in response to collagen type II was not altered. The production of IFN-gamma, TNF-alpha, and IL-1beta by LPS-stimulated spleen cells was decreased, and IL-10 was increased, in cells from Crry-Tg mice in comparison to WT. The steady-state mRNA levels for IFN-gamma, TNF-alpha, and IL-1beta were all decreased in the joints of Crry-Tg mice in comparison to WT. The synovium from Crry-Tg mice without CIA contained the mRNA for the Crry transgene, by RT-PCR, and the synovium from transgenic mice with CIA exhibited little deposition of C3 protein by immunohistological analysis. These results suggest that suppression of CIA in Crry-Tg mice may be due to enhanced synthesis of Crry locally in the joint with decreased production of proinflammatory cytokines.</abstract><cop>United States</cop><pub>Am Assoc Immnol</pub><pmid>12902517</pmid><doi>10.4049/jimmunol.171.4.2109</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Arthritis, Experimental - genetics Arthritis, Experimental - immunology Arthritis, Experimental - pathology Arthritis, Experimental - prevention & control Autoantibodies - biosynthesis Autoantibodies - blood Cattle Collagen Type II - administration & dosage Collagen Type II - immunology Complement Inactivator Proteins - genetics Cytokines - biosynthesis Female Hindlimb Immunoglobulin G - biosynthesis Immunoglobulin G - blood Immunohistochemistry Injections, Intradermal Lymph Nodes - cytology Lymph Nodes - immunology Lymphocyte Activation - genetics Lymphocyte Subsets - immunology Male Mice Mice, Inbred C57BL Mice, Transgenic Receptors, Complement - biosynthesis Receptors, Complement - genetics Receptors, Complement 3b - genetics RNA, Messenger - analysis Spleen - cytology Spleen - immunology Spleen - metabolism |
title | Prevention of Collagen-Induced Arthritis in Mice Transgenic for the Complement Inhibitor Complement Receptor 1-Related Gene/Protein y |
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