Inhibition and stimulation of LFA-1 and Mac-1 functions by antibodies against murine CD18. Evidence that the LFA-1 binding sites for ICAM-1, -2, and -3 are distinct
The murine CD18 monoclonal antibody (mAb) M18/2 was reported to inhibit lymphoma metastasis [Zahalka, M. A. et al. (1993) J. Immunol. 150, 4466]. To identify the pathways potentially blocked, we studied the effects of M18/2 compared with two new mAb against murine CD18, GAME‐46, and ‐245. Whereas th...
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| Veröffentlicht in: | Journal of leukocyte biology 1996-12, Vol.60 (6), p.758-765 |
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| creator | Driessens, Mariëtte H. E. Hulten, Paula Zuurbier, Astrid La Rivière, Geertje Roos, Ed |
| description | The murine CD18 monoclonal antibody (mAb) M18/2 was reported to inhibit lymphoma metastasis [Zahalka, M. A. et al. (1993) J. Immunol. 150, 4466]. To identify the pathways potentially blocked, we studied the effects of M18/2 compared with two new mAb against murine CD18, GAME‐46, and ‐245. Whereas the GAME mAb blocked most Mac‐l‐mediated interactions, M18/2 had no effect, or even stimulated. The same was true for adhesion of LFA‐1 to ICAM‐1. To test effects on interactions with different ICAMs, we used L cells transfected with human IGAM‐1, ‐2, and ‐3. As previously described, mouse LFA‐1 does not bind to human ICAM‐1 but we show here that mouse LFA‐1 does bind to human ICAM‐2 and ‐3. Again, the GAME mAb blocked completely, but M18/2 did not. These results indicate that the LFA‐1 binding sites for ICAM‐1 and ICAM‐2 and‐3, although in close vicinity, are distinct. Furthermore, effects of M18/2 on metastasis cannot be ascribed to blocking of any known β2‐integrin activity. J. Leukoc. Biol. 60: 758–765; 1996. |
| doi_str_mv | 10.1002/jlb.60.6.758 |
| format | Article |
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Evidence that the LFA-1 binding sites for ICAM-1, -2, and -3 are distinct</title><source>MEDLINE</source><source>Oxford University Press Journals All Titles (1996-Current)</source><creator>Driessens, Mariëtte H. E. ; Hulten, Paula ; Zuurbier, Astrid ; La Rivière, Geertje ; Roos, Ed</creator><creatorcontrib>Driessens, Mariëtte H. E. ; Hulten, Paula ; Zuurbier, Astrid ; La Rivière, Geertje ; Roos, Ed</creatorcontrib><description>The murine CD18 monoclonal antibody (mAb) M18/2 was reported to inhibit lymphoma metastasis [Zahalka, M. A. et al. (1993) J. Immunol. 150, 4466]. To identify the pathways potentially blocked, we studied the effects of M18/2 compared with two new mAb against murine CD18, GAME‐46, and ‐245. Whereas the GAME mAb blocked most Mac‐l‐mediated interactions, M18/2 had no effect, or even stimulated. The same was true for adhesion of LFA‐1 to ICAM‐1. To test effects on interactions with different ICAMs, we used L cells transfected with human IGAM‐1, ‐2, and ‐3. As previously described, mouse LFA‐1 does not bind to human ICAM‐1 but we show here that mouse LFA‐1 does bind to human ICAM‐2 and ‐3. Again, the GAME mAb blocked completely, but M18/2 did not. These results indicate that the LFA‐1 binding sites for ICAM‐1 and ICAM‐2 and‐3, although in close vicinity, are distinct. Furthermore, effects of M18/2 on metastasis cannot be ascribed to blocking of any known β2‐integrin activity. J. Leukoc. Biol. 60: 758–765; 1996.</description><identifier>ISSN: 0741-5400</identifier><identifier>EISSN: 1938-3673</identifier><identifier>DOI: 10.1002/jlb.60.6.758</identifier><identifier>PMID: 8975879</identifier><language>eng</language><publisher>United States: Society for Leukocyte Biology</publisher><subject>Animals ; Antibodies, Monoclonal - immunology ; Antigen-Antibody Reactions ; Antigens, CD - metabolism ; Antigens, Differentiation ; Binding Sites ; Binding, Competitive ; CD18 Antigens - metabolism ; CDlla ; Cell Adhesion ; Cell Adhesion Molecules - metabolism ; Complement C3b - metabolism ; Epitopes ; Fibrinogen - metabolism ; Gelatin - metabolism ; Humans ; Hybridomas ; Intercellular Adhesion Molecule-1 - metabolism ; leukocyte ; Lymphocyte Function-Associated Antigen-1 - metabolism ; Lymphoma - pathology ; Macrophage-1 Antigen - metabolism ; Mice ; mouse ; Neoplasm Metastasis ; Precipitin Tests ; Rats ; Species Specificity ; β2integrin</subject><ispartof>Journal of leukocyte biology, 1996-12, Vol.60 (6), p.758-765</ispartof><rights>1996 Society for Leukocyte Biology</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3898-cbc181320459b8d7d0c15bba002ff234d44a1835f029e7b5d23f24d44d01037f3</citedby></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/8975879$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Driessens, Mariëtte H. E.</creatorcontrib><creatorcontrib>Hulten, Paula</creatorcontrib><creatorcontrib>Zuurbier, Astrid</creatorcontrib><creatorcontrib>La Rivière, Geertje</creatorcontrib><creatorcontrib>Roos, Ed</creatorcontrib><title>Inhibition and stimulation of LFA-1 and Mac-1 functions by antibodies against murine CD18. Evidence that the LFA-1 binding sites for ICAM-1, -2, and -3 are distinct</title><title>Journal of leukocyte biology</title><addtitle>J Leukoc Biol</addtitle><description>The murine CD18 monoclonal antibody (mAb) M18/2 was reported to inhibit lymphoma metastasis [Zahalka, M. A. et al. (1993) J. Immunol. 150, 4466]. To identify the pathways potentially blocked, we studied the effects of M18/2 compared with two new mAb against murine CD18, GAME‐46, and ‐245. Whereas the GAME mAb blocked most Mac‐l‐mediated interactions, M18/2 had no effect, or even stimulated. The same was true for adhesion of LFA‐1 to ICAM‐1. To test effects on interactions with different ICAMs, we used L cells transfected with human IGAM‐1, ‐2, and ‐3. As previously described, mouse LFA‐1 does not bind to human ICAM‐1 but we show here that mouse LFA‐1 does bind to human ICAM‐2 and ‐3. Again, the GAME mAb blocked completely, but M18/2 did not. These results indicate that the LFA‐1 binding sites for ICAM‐1 and ICAM‐2 and‐3, although in close vicinity, are distinct. Furthermore, effects of M18/2 on metastasis cannot be ascribed to blocking of any known β2‐integrin activity. J. Leukoc. Biol. 60: 758–765; 1996.</description><subject>Animals</subject><subject>Antibodies, Monoclonal - immunology</subject><subject>Antigen-Antibody Reactions</subject><subject>Antigens, CD - metabolism</subject><subject>Antigens, Differentiation</subject><subject>Binding Sites</subject><subject>Binding, Competitive</subject><subject>CD18 Antigens - metabolism</subject><subject>CDlla</subject><subject>Cell Adhesion</subject><subject>Cell Adhesion Molecules - metabolism</subject><subject>Complement C3b - metabolism</subject><subject>Epitopes</subject><subject>Fibrinogen - metabolism</subject><subject>Gelatin - metabolism</subject><subject>Humans</subject><subject>Hybridomas</subject><subject>Intercellular Adhesion Molecule-1 - metabolism</subject><subject>leukocyte</subject><subject>Lymphocyte Function-Associated Antigen-1 - metabolism</subject><subject>Lymphoma - pathology</subject><subject>Macrophage-1 Antigen - metabolism</subject><subject>Mice</subject><subject>mouse</subject><subject>Neoplasm Metastasis</subject><subject>Precipitin Tests</subject><subject>Rats</subject><subject>Species Specificity</subject><subject>β2integrin</subject><issn>0741-5400</issn><issn>1938-3673</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFUU1v0zAYthBodIMbVyRf4NSE13YSO8dRtjHUiQucLTu2W0-JM-KEqP-HH4rbVDvCxR_v82X5QegdgZwA0E-Prc4ryKucl-IFWpGaiYxVnL1EK-AFycoC4DW6jPERABit4AJdiDqReb1Cf-7D3ms_-j5gFQyOo--mVp3uvcPb2-uMnIAH1aSTm0JzxCLWhzQeve6NtxGrnfIhjribBh8s3nwhIsc3v72xobF43KsxLfZsp30wPuxw9GOSun7A95vrh4yscUbXp7CMYTVYbHx6Tgp8g1451Ub79rxfoZ-3Nz82X7Pt97sk3WYNE7XIGt0QQRiFoqy1MNxAQ0qtVfok5ygrTFEoIljpgNaW69JQ5uhxaoAA445doY-L79PQ_5psHGXnY2PbVgXbT1FyUVEugP6XSMqaCsZJIq4XYjP0MQ7WyafBd2o4SALy2J5M7ckKZCVTIYn-_uw76c6aZ_K5roSTBZ99aw__9JLftp9h8fywaPZ-t5_9YGXsVNumBCrneX7O_gv0aa7N</recordid><startdate>199612</startdate><enddate>199612</enddate><creator>Driessens, Mariëtte H. E.</creator><creator>Hulten, Paula</creator><creator>Zuurbier, Astrid</creator><creator>La Rivière, Geertje</creator><creator>Roos, Ed</creator><general>Society for Leukocyte Biology</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>199612</creationdate><title>Inhibition and stimulation of LFA-1 and Mac-1 functions by antibodies against murine CD18. Evidence that the LFA-1 binding sites for ICAM-1, -2, and -3 are distinct</title><author>Driessens, Mariëtte H. E. ; Hulten, Paula ; Zuurbier, Astrid ; La Rivière, Geertje ; Roos, Ed</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3898-cbc181320459b8d7d0c15bba002ff234d44a1835f029e7b5d23f24d44d01037f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Animals</topic><topic>Antibodies, Monoclonal - immunology</topic><topic>Antigen-Antibody Reactions</topic><topic>Antigens, CD - metabolism</topic><topic>Antigens, Differentiation</topic><topic>Binding Sites</topic><topic>Binding, Competitive</topic><topic>CD18 Antigens - metabolism</topic><topic>CDlla</topic><topic>Cell Adhesion</topic><topic>Cell Adhesion Molecules - metabolism</topic><topic>Complement C3b - metabolism</topic><topic>Epitopes</topic><topic>Fibrinogen - metabolism</topic><topic>Gelatin - metabolism</topic><topic>Humans</topic><topic>Hybridomas</topic><topic>Intercellular Adhesion Molecule-1 - metabolism</topic><topic>leukocyte</topic><topic>Lymphocyte Function-Associated Antigen-1 - metabolism</topic><topic>Lymphoma - pathology</topic><topic>Macrophage-1 Antigen - metabolism</topic><topic>Mice</topic><topic>mouse</topic><topic>Neoplasm Metastasis</topic><topic>Precipitin Tests</topic><topic>Rats</topic><topic>Species Specificity</topic><topic>β2integrin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Driessens, Mariëtte H. E.</creatorcontrib><creatorcontrib>Hulten, Paula</creatorcontrib><creatorcontrib>Zuurbier, Astrid</creatorcontrib><creatorcontrib>La Rivière, Geertje</creatorcontrib><creatorcontrib>Roos, Ed</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 leukocyte biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Driessens, Mariëtte H. E.</au><au>Hulten, Paula</au><au>Zuurbier, Astrid</au><au>La Rivière, Geertje</au><au>Roos, Ed</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition and stimulation of LFA-1 and Mac-1 functions by antibodies against murine CD18. Evidence that the LFA-1 binding sites for ICAM-1, -2, and -3 are distinct</atitle><jtitle>Journal of leukocyte biology</jtitle><addtitle>J Leukoc Biol</addtitle><date>1996-12</date><risdate>1996</risdate><volume>60</volume><issue>6</issue><spage>758</spage><epage>765</epage><pages>758-765</pages><issn>0741-5400</issn><eissn>1938-3673</eissn><abstract>The murine CD18 monoclonal antibody (mAb) M18/2 was reported to inhibit lymphoma metastasis [Zahalka, M. A. et al. (1993) J. Immunol. 150, 4466]. To identify the pathways potentially blocked, we studied the effects of M18/2 compared with two new mAb against murine CD18, GAME‐46, and ‐245. Whereas the GAME mAb blocked most Mac‐l‐mediated interactions, M18/2 had no effect, or even stimulated. The same was true for adhesion of LFA‐1 to ICAM‐1. To test effects on interactions with different ICAMs, we used L cells transfected with human IGAM‐1, ‐2, and ‐3. As previously described, mouse LFA‐1 does not bind to human ICAM‐1 but we show here that mouse LFA‐1 does bind to human ICAM‐2 and ‐3. Again, the GAME mAb blocked completely, but M18/2 did not. These results indicate that the LFA‐1 binding sites for ICAM‐1 and ICAM‐2 and‐3, although in close vicinity, are distinct. Furthermore, effects of M18/2 on metastasis cannot be ascribed to blocking of any known β2‐integrin activity. J. Leukoc. Biol. 60: 758–765; 1996.</abstract><cop>United States</cop><pub>Society for Leukocyte Biology</pub><pmid>8975879</pmid><doi>10.1002/jlb.60.6.758</doi><tpages>8</tpages></addata></record> |
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| ispartof | Journal of leukocyte biology, 1996-12, Vol.60 (6), p.758-765 |
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| language | eng |
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| source | MEDLINE; Oxford University Press Journals All Titles (1996-Current) |
| subjects | Animals Antibodies, Monoclonal - immunology Antigen-Antibody Reactions Antigens, CD - metabolism Antigens, Differentiation Binding Sites Binding, Competitive CD18 Antigens - metabolism CDlla Cell Adhesion Cell Adhesion Molecules - metabolism Complement C3b - metabolism Epitopes Fibrinogen - metabolism Gelatin - metabolism Humans Hybridomas Intercellular Adhesion Molecule-1 - metabolism leukocyte Lymphocyte Function-Associated Antigen-1 - metabolism Lymphoma - pathology Macrophage-1 Antigen - metabolism Mice mouse Neoplasm Metastasis Precipitin Tests Rats Species Specificity β2integrin |
| title | Inhibition and stimulation of LFA-1 and Mac-1 functions by antibodies against murine CD18. Evidence that the LFA-1 binding sites for ICAM-1, -2, and -3 are distinct |
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