Antiinflammatory properties of a peptide derived from interleukin-4
•We report a novel synthetic peptide which mimics anti-inflammatory properties of IL-4.•The IL-4 mimetic is a partial agonist of the IL-4 receptor complex type I.•The IL-4 mimetic is an antagonist of the IL-4 receptor complex type II.•It delayed signs of chronic inflammation in collagen-induced arth...
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| Veröffentlicht in: | Cytokine (Philadelphia, Pa.) Pa.), 2013-10, Vol.64 (1), p.112-121 |
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| creator | Klementiev, Boris Enevoldsen, Maj N. Li, Shizhong Carlsson, Robert Liu, Yawei Issazadeh-Navikas, Shohreh Bock, Elisabeth Berezin, Vladimir |
| description | •We report a novel synthetic peptide which mimics anti-inflammatory properties of IL-4.•The IL-4 mimetic is a partial agonist of the IL-4 receptor complex type I.•The IL-4 mimetic is an antagonist of the IL-4 receptor complex type II.•It delayed signs of chronic inflammation in collagen-induced arthritis in rat.
Interleukin-4 (IL-4) is a potent antiinflammatory cytokine. However its use in the clinic is hampered by side effects. We here describe the identification of a novel synthetic peptide, termed Ph8, derived from α-helix C of IL-4, which interacts with IL-4 receptor α (IL-4Rα). Employing various cultured genetically engineered cell lines and primary lymphocytes, surface plasmon resonance, qPCR, ELISA and immunoblotting techniques we found that Ph8 bound IL-4Rα and mimicked the anti-inflammatory effects of IL-4 by inhibiting TNF-α production by macrophages in vitro. It induced phosphorylation of STAT6 65kD but inhibited phosphorylation of STAT6 110kD induced by IL-4 in a B-cell line that expressed the type I receptor. It also inhibited the IL-4-stimulated expression of a STAT6-inducible reporter gene in cells that expressed the type II receptor. Ph8 inhibited the proliferation of Th1/2 cells and downregulated the production of IFN-γ in stimulated Th1 cells. Moreover, Ph8 did not induce any shift in Th1/Th2 profile. This is a favorable effect and it is indicating that Ph8 could block general T cell activation and inflammatory responses without further inducing the side effects generally associated with IL-4 signaling. These data collectively show that Ph8 is only a partial agonist of IL-4 mimicking its desirable properties. In agreement, Ph8 treatment of rats with collagen-induced arthritis, a Th1- and antibody- mediated disease of joint, delayed the manifestation of chronic inflammation and reduced acute inflammation in carrageenan-induced edema. Our findings indicate that Ph8 is a promising potential drug candidate for the treatment of inflammatory diseases. |
| doi_str_mv | 10.1016/j.cyto.2013.07.016 |
| format | Article |
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Interleukin-4 (IL-4) is a potent antiinflammatory cytokine. However its use in the clinic is hampered by side effects. We here describe the identification of a novel synthetic peptide, termed Ph8, derived from α-helix C of IL-4, which interacts with IL-4 receptor α (IL-4Rα). Employing various cultured genetically engineered cell lines and primary lymphocytes, surface plasmon resonance, qPCR, ELISA and immunoblotting techniques we found that Ph8 bound IL-4Rα and mimicked the anti-inflammatory effects of IL-4 by inhibiting TNF-α production by macrophages in vitro. It induced phosphorylation of STAT6 65kD but inhibited phosphorylation of STAT6 110kD induced by IL-4 in a B-cell line that expressed the type I receptor. It also inhibited the IL-4-stimulated expression of a STAT6-inducible reporter gene in cells that expressed the type II receptor. Ph8 inhibited the proliferation of Th1/2 cells and downregulated the production of IFN-γ in stimulated Th1 cells. Moreover, Ph8 did not induce any shift in Th1/Th2 profile. This is a favorable effect and it is indicating that Ph8 could block general T cell activation and inflammatory responses without further inducing the side effects generally associated with IL-4 signaling. These data collectively show that Ph8 is only a partial agonist of IL-4 mimicking its desirable properties. In agreement, Ph8 treatment of rats with collagen-induced arthritis, a Th1- and antibody- mediated disease of joint, delayed the manifestation of chronic inflammation and reduced acute inflammation in carrageenan-induced edema. Our findings indicate that Ph8 is a promising potential drug candidate for the treatment of inflammatory diseases.</description><identifier>ISSN: 1043-4666</identifier><identifier>EISSN: 1096-0023</identifier><identifier>DOI: 10.1016/j.cyto.2013.07.016</identifier><identifier>PMID: 23972727</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>adverse effects ; agonists ; Animals ; anti-inflammatory activity ; Anti-Inflammatory Agents, Non-Steroidal - pharmacology ; arthritis ; Arthritis, Experimental - drug therapy ; B-lymphocytes ; Cell Proliferation - drug effects ; Collagen-induced arthritis ; drugs ; edema ; Edema - drug therapy ; HEK293 Cells ; Humans ; immunoblotting ; inflammation ; Interferon-gamma - metabolism ; Interferon-γ ; Interleukin-4 ; Interleukin-4 - analogs & derivatives ; Interleukin-4 - chemistry ; Interleukin-4 - pharmacology ; Interleukin-4 Receptor alpha Subunit - metabolism ; Lymphocyte Activation - drug effects ; Lymphocyte Activation - immunology ; Macrophage Activation - drug effects ; macrophages ; Macrophages - drug effects ; Macrophages - metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Peptide Fragments - chemistry ; Peptide Fragments - pharmacology ; phosphorylation ; Phosphorylation - drug effects ; Protein Binding ; Rats ; Rats, Wistar ; reporter genes ; Signalling ; STAT6 Transcription Factor - metabolism ; surface plasmon resonance ; Th1 Cells - drug effects ; Th1 Cells - metabolism ; Tumor Necrosis Factor-alpha - biosynthesis ; Tumor necrosis factor-α</subject><ispartof>Cytokine (Philadelphia, Pa.), 2013-10, Vol.64 (1), p.112-121</ispartof><rights>2013 Elsevier Ltd</rights><rights>Copyright © 2013 Elsevier Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c413t-6a66b242994fd96390020823410923106b7416392201316030fbf5774c45c8aa3</citedby><cites>FETCH-LOGICAL-c413t-6a66b242994fd96390020823410923106b7416392201316030fbf5774c45c8aa3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1043466613006315$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23972727$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Klementiev, Boris</creatorcontrib><creatorcontrib>Enevoldsen, Maj N.</creatorcontrib><creatorcontrib>Li, Shizhong</creatorcontrib><creatorcontrib>Carlsson, Robert</creatorcontrib><creatorcontrib>Liu, Yawei</creatorcontrib><creatorcontrib>Issazadeh-Navikas, Shohreh</creatorcontrib><creatorcontrib>Bock, Elisabeth</creatorcontrib><creatorcontrib>Berezin, Vladimir</creatorcontrib><title>Antiinflammatory properties of a peptide derived from interleukin-4</title><title>Cytokine (Philadelphia, Pa.)</title><addtitle>Cytokine</addtitle><description>•We report a novel synthetic peptide which mimics anti-inflammatory properties of IL-4.•The IL-4 mimetic is a partial agonist of the IL-4 receptor complex type I.•The IL-4 mimetic is an antagonist of the IL-4 receptor complex type II.•It delayed signs of chronic inflammation in collagen-induced arthritis in rat.
Interleukin-4 (IL-4) is a potent antiinflammatory cytokine. However its use in the clinic is hampered by side effects. We here describe the identification of a novel synthetic peptide, termed Ph8, derived from α-helix C of IL-4, which interacts with IL-4 receptor α (IL-4Rα). Employing various cultured genetically engineered cell lines and primary lymphocytes, surface plasmon resonance, qPCR, ELISA and immunoblotting techniques we found that Ph8 bound IL-4Rα and mimicked the anti-inflammatory effects of IL-4 by inhibiting TNF-α production by macrophages in vitro. It induced phosphorylation of STAT6 65kD but inhibited phosphorylation of STAT6 110kD induced by IL-4 in a B-cell line that expressed the type I receptor. It also inhibited the IL-4-stimulated expression of a STAT6-inducible reporter gene in cells that expressed the type II receptor. Ph8 inhibited the proliferation of Th1/2 cells and downregulated the production of IFN-γ in stimulated Th1 cells. Moreover, Ph8 did not induce any shift in Th1/Th2 profile. This is a favorable effect and it is indicating that Ph8 could block general T cell activation and inflammatory responses without further inducing the side effects generally associated with IL-4 signaling. These data collectively show that Ph8 is only a partial agonist of IL-4 mimicking its desirable properties. In agreement, Ph8 treatment of rats with collagen-induced arthritis, a Th1- and antibody- mediated disease of joint, delayed the manifestation of chronic inflammation and reduced acute inflammation in carrageenan-induced edema. Our findings indicate that Ph8 is a promising potential drug candidate for the treatment of inflammatory diseases.</description><subject>adverse effects</subject><subject>agonists</subject><subject>Animals</subject><subject>anti-inflammatory activity</subject><subject>Anti-Inflammatory Agents, Non-Steroidal - pharmacology</subject><subject>arthritis</subject><subject>Arthritis, Experimental - drug therapy</subject><subject>B-lymphocytes</subject><subject>Cell Proliferation - drug effects</subject><subject>Collagen-induced arthritis</subject><subject>drugs</subject><subject>edema</subject><subject>Edema - drug therapy</subject><subject>HEK293 Cells</subject><subject>Humans</subject><subject>immunoblotting</subject><subject>inflammation</subject><subject>Interferon-gamma - metabolism</subject><subject>Interferon-γ</subject><subject>Interleukin-4</subject><subject>Interleukin-4 - analogs & derivatives</subject><subject>Interleukin-4 - chemistry</subject><subject>Interleukin-4 - pharmacology</subject><subject>Interleukin-4 Receptor alpha Subunit - metabolism</subject><subject>Lymphocyte Activation - drug effects</subject><subject>Lymphocyte Activation - immunology</subject><subject>Macrophage Activation - drug effects</subject><subject>macrophages</subject><subject>Macrophages - drug effects</subject><subject>Macrophages - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Peptide Fragments - chemistry</subject><subject>Peptide Fragments - pharmacology</subject><subject>phosphorylation</subject><subject>Phosphorylation - drug effects</subject><subject>Protein Binding</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>reporter genes</subject><subject>Signalling</subject><subject>STAT6 Transcription Factor - metabolism</subject><subject>surface plasmon resonance</subject><subject>Th1 Cells - drug effects</subject><subject>Th1 Cells - metabolism</subject><subject>Tumor Necrosis Factor-alpha - biosynthesis</subject><subject>Tumor necrosis factor-α</subject><issn>1043-4666</issn><issn>1096-0023</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkEtv1DAUhS1URB_wB1hAlt0kXD9iJ1I31ailSJVYQNeWx7lGHpI4tT0jzb_H0ZQuQV7YOvruuceHkI8UGgpUftk19phDw4DyBlRTpDfkgkIvawDGz9a34LWQUp6Ty5R2ANBzpd6Rc8Z7xcq5IJvbOXs_u9FMk8khHqslhgVj9piq4CpTLbhkP2A1YPQHHCoXw1T5OWMccf_bz7V4T946Myb88HJfkaf7u5-bh_rx-9dvm9vH2grKcy2NlFsmWN8LN_SS9yUldIyLEplxCnKrBC0yWz9EJXBwW9cqJaxobWcMvyLXJ98S8XmPKevJJ4vjaGYM-6RpC6Dajsvu_6goGxjvFC8oO6E2hpQiOr1EP5l41BT02rPe6bVnvcbSoHSRytCnF__9dsLhdeRvsQX4fAKcCdr8ij7ppx_FoUSErm3FuvfmRGCp7OAx6mQ9zhYHH9FmPQT_rwR_AJx7lOM</recordid><startdate>20131001</startdate><enddate>20131001</enddate><creator>Klementiev, Boris</creator><creator>Enevoldsen, Maj N.</creator><creator>Li, Shizhong</creator><creator>Carlsson, Robert</creator><creator>Liu, Yawei</creator><creator>Issazadeh-Navikas, Shohreh</creator><creator>Bock, Elisabeth</creator><creator>Berezin, Vladimir</creator><general>Elsevier Ltd</general><scope>FBQ</scope><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>7X8</scope><scope>7T5</scope><scope>H94</scope></search><sort><creationdate>20131001</creationdate><title>Antiinflammatory properties of a peptide derived from interleukin-4</title><author>Klementiev, Boris ; Enevoldsen, Maj N. ; Li, Shizhong ; Carlsson, Robert ; Liu, Yawei ; Issazadeh-Navikas, Shohreh ; Bock, Elisabeth ; Berezin, Vladimir</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c413t-6a66b242994fd96390020823410923106b7416392201316030fbf5774c45c8aa3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>adverse effects</topic><topic>agonists</topic><topic>Animals</topic><topic>anti-inflammatory activity</topic><topic>Anti-Inflammatory Agents, Non-Steroidal - pharmacology</topic><topic>arthritis</topic><topic>Arthritis, Experimental - drug therapy</topic><topic>B-lymphocytes</topic><topic>Cell Proliferation - drug effects</topic><topic>Collagen-induced arthritis</topic><topic>drugs</topic><topic>edema</topic><topic>Edema - drug therapy</topic><topic>HEK293 Cells</topic><topic>Humans</topic><topic>immunoblotting</topic><topic>inflammation</topic><topic>Interferon-gamma - metabolism</topic><topic>Interferon-γ</topic><topic>Interleukin-4</topic><topic>Interleukin-4 - analogs & derivatives</topic><topic>Interleukin-4 - chemistry</topic><topic>Interleukin-4 - pharmacology</topic><topic>Interleukin-4 Receptor alpha Subunit - metabolism</topic><topic>Lymphocyte Activation - drug effects</topic><topic>Lymphocyte Activation - immunology</topic><topic>Macrophage Activation - drug effects</topic><topic>macrophages</topic><topic>Macrophages - drug effects</topic><topic>Macrophages - metabolism</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Peptide Fragments - chemistry</topic><topic>Peptide Fragments - pharmacology</topic><topic>phosphorylation</topic><topic>Phosphorylation - drug effects</topic><topic>Protein Binding</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>reporter genes</topic><topic>Signalling</topic><topic>STAT6 Transcription Factor - metabolism</topic><topic>surface plasmon resonance</topic><topic>Th1 Cells - drug effects</topic><topic>Th1 Cells - metabolism</topic><topic>Tumor Necrosis Factor-alpha - biosynthesis</topic><topic>Tumor necrosis factor-α</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Klementiev, Boris</creatorcontrib><creatorcontrib>Enevoldsen, Maj N.</creatorcontrib><creatorcontrib>Li, Shizhong</creatorcontrib><creatorcontrib>Carlsson, Robert</creatorcontrib><creatorcontrib>Liu, Yawei</creatorcontrib><creatorcontrib>Issazadeh-Navikas, Shohreh</creatorcontrib><creatorcontrib>Bock, Elisabeth</creatorcontrib><creatorcontrib>Berezin, Vladimir</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Cytokine (Philadelphia, Pa.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Klementiev, Boris</au><au>Enevoldsen, Maj N.</au><au>Li, Shizhong</au><au>Carlsson, Robert</au><au>Liu, Yawei</au><au>Issazadeh-Navikas, Shohreh</au><au>Bock, Elisabeth</au><au>Berezin, Vladimir</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Antiinflammatory properties of a peptide derived from interleukin-4</atitle><jtitle>Cytokine (Philadelphia, Pa.)</jtitle><addtitle>Cytokine</addtitle><date>2013-10-01</date><risdate>2013</risdate><volume>64</volume><issue>1</issue><spage>112</spage><epage>121</epage><pages>112-121</pages><issn>1043-4666</issn><eissn>1096-0023</eissn><abstract>•We report a novel synthetic peptide which mimics anti-inflammatory properties of IL-4.•The IL-4 mimetic is a partial agonist of the IL-4 receptor complex type I.•The IL-4 mimetic is an antagonist of the IL-4 receptor complex type II.•It delayed signs of chronic inflammation in collagen-induced arthritis in rat.
Interleukin-4 (IL-4) is a potent antiinflammatory cytokine. However its use in the clinic is hampered by side effects. We here describe the identification of a novel synthetic peptide, termed Ph8, derived from α-helix C of IL-4, which interacts with IL-4 receptor α (IL-4Rα). Employing various cultured genetically engineered cell lines and primary lymphocytes, surface plasmon resonance, qPCR, ELISA and immunoblotting techniques we found that Ph8 bound IL-4Rα and mimicked the anti-inflammatory effects of IL-4 by inhibiting TNF-α production by macrophages in vitro. It induced phosphorylation of STAT6 65kD but inhibited phosphorylation of STAT6 110kD induced by IL-4 in a B-cell line that expressed the type I receptor. It also inhibited the IL-4-stimulated expression of a STAT6-inducible reporter gene in cells that expressed the type II receptor. Ph8 inhibited the proliferation of Th1/2 cells and downregulated the production of IFN-γ in stimulated Th1 cells. Moreover, Ph8 did not induce any shift in Th1/Th2 profile. This is a favorable effect and it is indicating that Ph8 could block general T cell activation and inflammatory responses without further inducing the side effects generally associated with IL-4 signaling. These data collectively show that Ph8 is only a partial agonist of IL-4 mimicking its desirable properties. In agreement, Ph8 treatment of rats with collagen-induced arthritis, a Th1- and antibody- mediated disease of joint, delayed the manifestation of chronic inflammation and reduced acute inflammation in carrageenan-induced edema. Our findings indicate that Ph8 is a promising potential drug candidate for the treatment of inflammatory diseases.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>23972727</pmid><doi>10.1016/j.cyto.2013.07.016</doi><tpages>10</tpages></addata></record> |
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| subjects | adverse effects agonists Animals anti-inflammatory activity Anti-Inflammatory Agents, Non-Steroidal - pharmacology arthritis Arthritis, Experimental - drug therapy B-lymphocytes Cell Proliferation - drug effects Collagen-induced arthritis drugs edema Edema - drug therapy HEK293 Cells Humans immunoblotting inflammation Interferon-gamma - metabolism Interferon-γ Interleukin-4 Interleukin-4 - analogs & derivatives Interleukin-4 - chemistry Interleukin-4 - pharmacology Interleukin-4 Receptor alpha Subunit - metabolism Lymphocyte Activation - drug effects Lymphocyte Activation - immunology Macrophage Activation - drug effects macrophages Macrophages - drug effects Macrophages - metabolism Male Mice Mice, Inbred C57BL Peptide Fragments - chemistry Peptide Fragments - pharmacology phosphorylation Phosphorylation - drug effects Protein Binding Rats Rats, Wistar reporter genes Signalling STAT6 Transcription Factor - metabolism surface plasmon resonance Th1 Cells - drug effects Th1 Cells - metabolism Tumor Necrosis Factor-alpha - biosynthesis Tumor necrosis factor-α |
| title | Antiinflammatory properties of a peptide derived from interleukin-4 |
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