Vaccination with cell immunoglobulin mucin‐1 antibodies and inactivated influenza enhances vaccine‐specific lymphocyte proliferation, interferon‐γ production and cross‐strain reactivity

Summary Influenza virus causes a contagious and potentially serious infection of the upper respiratory tract. While neutralizing antibodies are protective against infection, the problem of antigenic drift remains, requiring the constant monitoring and development of new vaccines. The magnitude of th...

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Veröffentlicht in:Clinical and experimental immunology 2006-07, Vol.145 (1), p.123-129
Hauptverfasser: Soo Hoo, W., Jensen, E. R., Saadat, A., Nieto, D., Moss, R. B., Carlo, D. J., Moll, T.
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container_end_page 129
container_issue 1
container_start_page 123
container_title Clinical and experimental immunology
container_volume 145
creator Soo Hoo, W.
Jensen, E. R.
Saadat, A.
Nieto, D.
Moss, R. B.
Carlo, D. J.
Moll, T.
description Summary Influenza virus causes a contagious and potentially serious infection of the upper respiratory tract. While neutralizing antibodies are protective against infection, the problem of antigenic drift remains, requiring the constant monitoring and development of new vaccines. The magnitude of this situation is underscored by the emergence of new potentially human pathogenic influenza strains, avian H5N1 being the most recent example. We present evidence that antibodies against T cell immunoglobulin mucin‐1 (TIM‐1), a recently identified immunomodulatory molecule, stimulate cellular immunity against influenza viruses and cross‐strain immune reactivity. To determine potential immunostimulatory properties of anti‐TIM‐1, mice were vaccinated with inactivated influenza virus in the presence or absence of TIM‐1‐specific monoclonal antibodies. Development of cellular immunity against both the influenza strain used for immunization and serotypically distinct virus strains was monitored 3 weeks after vaccination by determining antigen‐specific lymphocyte proliferation and cytokine production. Results show that TIM‐1 antibodies enhance antigen‐specific cellular proliferation (P 
doi_str_mv 10.1046/j.1365-2249.1998.00503.x-i1
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R. ; Saadat, A. ; Nieto, D. ; Moss, R. B. ; Carlo, D. J. ; Moll, T.</creator><creatorcontrib>Soo Hoo, W. ; Jensen, E. R. ; Saadat, A. ; Nieto, D. ; Moss, R. B. ; Carlo, D. J. ; Moll, T.</creatorcontrib><description>Summary Influenza virus causes a contagious and potentially serious infection of the upper respiratory tract. While neutralizing antibodies are protective against infection, the problem of antigenic drift remains, requiring the constant monitoring and development of new vaccines. The magnitude of this situation is underscored by the emergence of new potentially human pathogenic influenza strains, avian H5N1 being the most recent example. We present evidence that antibodies against T cell immunoglobulin mucin‐1 (TIM‐1), a recently identified immunomodulatory molecule, stimulate cellular immunity against influenza viruses and cross‐strain immune reactivity. To determine potential immunostimulatory properties of anti‐TIM‐1, mice were vaccinated with inactivated influenza virus in the presence or absence of TIM‐1‐specific monoclonal antibodies. Development of cellular immunity against both the influenza strain used for immunization and serotypically distinct virus strains was monitored 3 weeks after vaccination by determining antigen‐specific lymphocyte proliferation and cytokine production. Results show that TIM‐1 antibodies enhance antigen‐specific cellular proliferation (P &lt; 0·05) and interferon (IFN)‐γ production (P &lt; 0·01). Using blocking anti‐CD4 and CD8 antibodies, it was observed that antigen‐specific cellular proliferation is CD4‐dependent and that the majority of proliferating cells are CD4+. Finally, vaccination with inactivated influenza virus with TIM‐1 antibody results in the significant (P &lt; 0·001) induction of proliferation and IFN‐γ production upon stimulation with one of three serologically distinct strains. TIM‐1 antibodies demonstrate an adjuvant effect promoting antigen‐specific cellular proliferation and IFN‐γ production, which are important for the promotion of cell‐mediated immunity. These results are the first to suggest that TIM‐1 antibody may serve as a potent adjuvant in the development of new influenza virus vaccines.</description><identifier>ISSN: 0009-9104</identifier><identifier>EISSN: 1365-2249</identifier><identifier>DOI: 10.1046/j.1365-2249.1998.00503.x-i1</identifier><identifier>PMID: 16792682</identifier><identifier>CODEN: CEXIAL</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>adjuvant ; Adjuvants, Immunologic - administration &amp; dosage ; Animals ; Antibodies - administration &amp; dosage ; Biological and medical sciences ; CD4-Positive T-Lymphocytes - immunology ; Cell Proliferation ; Cross Reactions ; Cytokines - immunology ; Dose-Response Relationship, Drug ; Female ; Fundamental and applied biological sciences. 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We present evidence that antibodies against T cell immunoglobulin mucin‐1 (TIM‐1), a recently identified immunomodulatory molecule, stimulate cellular immunity against influenza viruses and cross‐strain immune reactivity. To determine potential immunostimulatory properties of anti‐TIM‐1, mice were vaccinated with inactivated influenza virus in the presence or absence of TIM‐1‐specific monoclonal antibodies. Development of cellular immunity against both the influenza strain used for immunization and serotypically distinct virus strains was monitored 3 weeks after vaccination by determining antigen‐specific lymphocyte proliferation and cytokine production. Results show that TIM‐1 antibodies enhance antigen‐specific cellular proliferation (P &lt; 0·05) and interferon (IFN)‐γ production (P &lt; 0·01). Using blocking anti‐CD4 and CD8 antibodies, it was observed that antigen‐specific cellular proliferation is CD4‐dependent and that the majority of proliferating cells are CD4+. Finally, vaccination with inactivated influenza virus with TIM‐1 antibody results in the significant (P &lt; 0·001) induction of proliferation and IFN‐γ production upon stimulation with one of three serologically distinct strains. TIM‐1 antibodies demonstrate an adjuvant effect promoting antigen‐specific cellular proliferation and IFN‐γ production, which are important for the promotion of cell‐mediated immunity. 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J.</au><au>Moll, T.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Vaccination with cell immunoglobulin mucin‐1 antibodies and inactivated influenza enhances vaccine‐specific lymphocyte proliferation, interferon‐γ production and cross‐strain reactivity</atitle><jtitle>Clinical and experimental immunology</jtitle><addtitle>Clin Exp Immunol</addtitle><date>2006-07</date><risdate>2006</risdate><volume>145</volume><issue>1</issue><spage>123</spage><epage>129</epage><pages>123-129</pages><issn>0009-9104</issn><eissn>1365-2249</eissn><coden>CEXIAL</coden><abstract>Summary Influenza virus causes a contagious and potentially serious infection of the upper respiratory tract. While neutralizing antibodies are protective against infection, the problem of antigenic drift remains, requiring the constant monitoring and development of new vaccines. The magnitude of this situation is underscored by the emergence of new potentially human pathogenic influenza strains, avian H5N1 being the most recent example. We present evidence that antibodies against T cell immunoglobulin mucin‐1 (TIM‐1), a recently identified immunomodulatory molecule, stimulate cellular immunity against influenza viruses and cross‐strain immune reactivity. To determine potential immunostimulatory properties of anti‐TIM‐1, mice were vaccinated with inactivated influenza virus in the presence or absence of TIM‐1‐specific monoclonal antibodies. Development of cellular immunity against both the influenza strain used for immunization and serotypically distinct virus strains was monitored 3 weeks after vaccination by determining antigen‐specific lymphocyte proliferation and cytokine production. Results show that TIM‐1 antibodies enhance antigen‐specific cellular proliferation (P &lt; 0·05) and interferon (IFN)‐γ production (P &lt; 0·01). Using blocking anti‐CD4 and CD8 antibodies, it was observed that antigen‐specific cellular proliferation is CD4‐dependent and that the majority of proliferating cells are CD4+. Finally, vaccination with inactivated influenza virus with TIM‐1 antibody results in the significant (P &lt; 0·001) induction of proliferation and IFN‐γ production upon stimulation with one of three serologically distinct strains. TIM‐1 antibodies demonstrate an adjuvant effect promoting antigen‐specific cellular proliferation and IFN‐γ production, which are important for the promotion of cell‐mediated immunity. These results are the first to suggest that TIM‐1 antibody may serve as a potent adjuvant in the development of new influenza virus vaccines.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>16792682</pmid><doi>10.1046/j.1365-2249.1998.00503.x-i1</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record>
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source PubMed Central (Open access); MEDLINE; Oxford Academic Journals (OUP); Alma/SFX Local Collection; EZB Electronic Journals Library
subjects adjuvant
Adjuvants, Immunologic - administration & dosage
Animals
Antibodies - administration & dosage
Biological and medical sciences
CD4-Positive T-Lymphocytes - immunology
Cell Proliferation
Cross Reactions
Cytokines - immunology
Dose-Response Relationship, Drug
Female
Fundamental and applied biological sciences. Psychology
Fundamental immunology
Hepatitis A Virus Cellular Receptor 1
heterosubtypic
IFN‐γ
Immunization
Immunopathology
influenza
Influenza Vaccines - administration & dosage
Injections, Intraperitoneal
Interferon-gamma - immunology
Medical sciences
Membrane Proteins - immunology
Mice
Mice, Inbred BALB C
Orthomyxoviridae - genetics
Orthomyxoviridae - immunology
TIM‐1
Vaccines, Attenuated - administration & dosage
title Vaccination with cell immunoglobulin mucin‐1 antibodies and inactivated influenza enhances vaccine‐specific lymphocyte proliferation, interferon‐γ production and cross‐strain reactivity
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