Burn injury primes naive CD4+ T cells for an augmented T-helper 1 response
Background: The mechanisms responsible for altered T-cell responses and cytokine production after injury are not well understood. We used T-cell receptor (TCR) transgenic mice to study burn injury effects on naive versus antigen-activated CD4+ T cells in vivo. Methods: One week after sham or burn in...
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Veröffentlicht in: | Surgery 1998-08, Vol.124 (2), p.269-277 |
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description | Background: The mechanisms responsible for altered T-cell responses and cytokine production after injury are not well understood. We used T-cell receptor (TCR) transgenic mice to study burn injury effects on naive versus antigen-activated CD4+ T cells in vivo.
Methods: One week after sham or burn injury, lymph node cells were prepared from TCR transgenic mice and stimulated with TCR transgene-specific antigens. T-cell proliferation was measured and culture supernatants were tested for interleukin-2 (IL-2), interferon-γ (IFN-γ), IL-4, and IL-10 by enzyme-linked immunosorbent assay (ELISA). Burn injury effects on antigen-activated T cells were studied by immunizing TCR transgenic or wild-type mice at the time of injury.
Results: The antigen-stimulated proliferation of naive CD4+ T cells was unaffected by burn injury and no increase in T-helper 2 (Th2)-type cytokine production was observed. Instead, burn injury augmented IFN-γ production by naive CD4+ transgenic T cells, and IL-2 production was marginally reduced. Thus, burn injury primed naive T cells for an enhanced Th1-type response. In contrast, antigen-specific proliferation, IL-2, and IFN-γ production by T cells harvested from immunized wild-type mice were suppressed. Unexpectedly, high mortality was observed when burn-injured TCR transgenic mice were immunized.
Conclusion: Our results show that burn injury has differential effects on naive and antigen-activated CD4+ T cells and can prime naive CD4+ T cells. (Surgery 1998;124:269-77.) |
doi_str_mv | 10.1016/S0039-6060(98)70130-8 |
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Methods: One week after sham or burn injury, lymph node cells were prepared from TCR transgenic mice and stimulated with TCR transgene-specific antigens. T-cell proliferation was measured and culture supernatants were tested for interleukin-2 (IL-2), interferon-γ (IFN-γ), IL-4, and IL-10 by enzyme-linked immunosorbent assay (ELISA). Burn injury effects on antigen-activated T cells were studied by immunizing TCR transgenic or wild-type mice at the time of injury.
Results: The antigen-stimulated proliferation of naive CD4+ T cells was unaffected by burn injury and no increase in T-helper 2 (Th2)-type cytokine production was observed. Instead, burn injury augmented IFN-γ production by naive CD4+ transgenic T cells, and IL-2 production was marginally reduced. Thus, burn injury primed naive T cells for an enhanced Th1-type response. In contrast, antigen-specific proliferation, IL-2, and IFN-γ production by T cells harvested from immunized wild-type mice were suppressed. Unexpectedly, high mortality was observed when burn-injured TCR transgenic mice were immunized.
Conclusion: Our results show that burn injury has differential effects on naive and antigen-activated CD4+ T cells and can prime naive CD4+ T cells. (Surgery 1998;124:269-77.)</description><identifier>ISSN: 0039-6060</identifier><identifier>EISSN: 1532-7361</identifier><identifier>DOI: 10.1016/S0039-6060(98)70130-8</identifier><identifier>PMID: 9706148</identifier><language>eng</language><publisher>United States: Mosby, Inc</publisher><subject>Animals ; Antigen Presentation - immunology ; Antigens - immunology ; Burns - immunology ; Burns - metabolism ; CD4-Positive T-Lymphocytes - cytology ; CD4-Positive T-Lymphocytes - immunology ; CD4-Positive T-Lymphocytes - metabolism ; Cell Division - immunology ; Disease Models, Animal ; Interferon-gamma - biosynthesis ; Interleukin-10 - biosynthesis ; Interleukin-4 - biosynthesis ; Lymphocyte Activation - immunology ; Male ; Mice ; Mice, Inbred A ; Mice, Transgenic ; Ovalbumin - biosynthesis</subject><ispartof>Surgery, 1998-08, Vol.124 (2), p.269-277</ispartof><rights>1998 Mosby, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c360t-52da7b3c3250514f02e082804aacefee7f56fcf5f5c8ac09f35b724f6fb14aba3</citedby><cites>FETCH-LOGICAL-c360t-52da7b3c3250514f02e082804aacefee7f56fcf5f5c8ac09f35b724f6fb14aba3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0039-6060(98)70130-8$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9706148$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kavanagh, Eamon G.</creatorcontrib><creatorcontrib>Kelly, John L.</creatorcontrib><creatorcontrib>Lyons, Ann</creatorcontrib><creatorcontrib>Soberg, Christopher C.</creatorcontrib><creatorcontrib>Mannick, John A.</creatorcontrib><creatorcontrib>Lederer, James A.</creatorcontrib><title>Burn injury primes naive CD4+ T cells for an augmented T-helper 1 response</title><title>Surgery</title><addtitle>Surgery</addtitle><description>Background: The mechanisms responsible for altered T-cell responses and cytokine production after injury are not well understood. We used T-cell receptor (TCR) transgenic mice to study burn injury effects on naive versus antigen-activated CD4+ T cells in vivo.
Methods: One week after sham or burn injury, lymph node cells were prepared from TCR transgenic mice and stimulated with TCR transgene-specific antigens. T-cell proliferation was measured and culture supernatants were tested for interleukin-2 (IL-2), interferon-γ (IFN-γ), IL-4, and IL-10 by enzyme-linked immunosorbent assay (ELISA). Burn injury effects on antigen-activated T cells were studied by immunizing TCR transgenic or wild-type mice at the time of injury.
Results: The antigen-stimulated proliferation of naive CD4+ T cells was unaffected by burn injury and no increase in T-helper 2 (Th2)-type cytokine production was observed. Instead, burn injury augmented IFN-γ production by naive CD4+ transgenic T cells, and IL-2 production was marginally reduced. Thus, burn injury primed naive T cells for an enhanced Th1-type response. In contrast, antigen-specific proliferation, IL-2, and IFN-γ production by T cells harvested from immunized wild-type mice were suppressed. Unexpectedly, high mortality was observed when burn-injured TCR transgenic mice were immunized.
Conclusion: Our results show that burn injury has differential effects on naive and antigen-activated CD4+ T cells and can prime naive CD4+ T cells. (Surgery 1998;124:269-77.)</description><subject>Animals</subject><subject>Antigen Presentation - immunology</subject><subject>Antigens - immunology</subject><subject>Burns - immunology</subject><subject>Burns - metabolism</subject><subject>CD4-Positive T-Lymphocytes - cytology</subject><subject>CD4-Positive T-Lymphocytes - immunology</subject><subject>CD4-Positive T-Lymphocytes - metabolism</subject><subject>Cell Division - immunology</subject><subject>Disease Models, Animal</subject><subject>Interferon-gamma - biosynthesis</subject><subject>Interleukin-10 - biosynthesis</subject><subject>Interleukin-4 - biosynthesis</subject><subject>Lymphocyte Activation - immunology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred A</subject><subject>Mice, Transgenic</subject><subject>Ovalbumin - biosynthesis</subject><issn>0039-6060</issn><issn>1532-7361</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkM1OwzAQhC0EKqXwCJV8QiAUWMex45wQlH9V4kA5W46zhlRtUuykUt-epK24ctrDzOzsfoSMGVwzYPLmA4BnkQQJF5m6TIFxiNQBGTLB4yjlkh2S4Z_lmJyEMAeALGFqQAZZCpIlakje7ltf0bKat35DV75cYqCVKddIJw_JFZ1Ri4tFoK721FTUtF9LrBos6Cz6xsUKPWXUY1jVVcBTcuTMIuDZfo7I59PjbPISTd-fXyd308hyCU0k4sKkObc8FiBY4iBGULGCxBiLDjF1QjrrhBNWGQuZ4yJP48RJl7PE5IaPyPlu78rXPy2GRi_L0J9pKqzboFOuZJwp1hnFzmh9HYJHp_sHjd9oBrpnqLcMdQ9IZ0pvGWrV5cb7gjZfYvGX2kPr9Nudjt2X6xK9DrbEymJRerSNLuryn4ZfnPB__g</recordid><startdate>19980801</startdate><enddate>19980801</enddate><creator>Kavanagh, Eamon G.</creator><creator>Kelly, John L.</creator><creator>Lyons, Ann</creator><creator>Soberg, Christopher C.</creator><creator>Mannick, John A.</creator><creator>Lederer, James A.</creator><general>Mosby, Inc</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>7X8</scope></search><sort><creationdate>19980801</creationdate><title>Burn injury primes naive CD4+ T cells for an augmented T-helper 1 response</title><author>Kavanagh, Eamon G. ; Kelly, John L. ; Lyons, Ann ; Soberg, Christopher C. ; Mannick, John A. ; Lederer, James A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c360t-52da7b3c3250514f02e082804aacefee7f56fcf5f5c8ac09f35b724f6fb14aba3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Animals</topic><topic>Antigen Presentation - immunology</topic><topic>Antigens - immunology</topic><topic>Burns - immunology</topic><topic>Burns - metabolism</topic><topic>CD4-Positive T-Lymphocytes - cytology</topic><topic>CD4-Positive T-Lymphocytes - immunology</topic><topic>CD4-Positive T-Lymphocytes - metabolism</topic><topic>Cell Division - immunology</topic><topic>Disease Models, Animal</topic><topic>Interferon-gamma - biosynthesis</topic><topic>Interleukin-10 - biosynthesis</topic><topic>Interleukin-4 - biosynthesis</topic><topic>Lymphocyte Activation - immunology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred A</topic><topic>Mice, Transgenic</topic><topic>Ovalbumin - biosynthesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kavanagh, Eamon G.</creatorcontrib><creatorcontrib>Kelly, John L.</creatorcontrib><creatorcontrib>Lyons, Ann</creatorcontrib><creatorcontrib>Soberg, Christopher C.</creatorcontrib><creatorcontrib>Mannick, John A.</creatorcontrib><creatorcontrib>Lederer, James A.</creatorcontrib><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><jtitle>Surgery</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kavanagh, Eamon G.</au><au>Kelly, John L.</au><au>Lyons, Ann</au><au>Soberg, Christopher C.</au><au>Mannick, John A.</au><au>Lederer, James A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Burn injury primes naive CD4+ T cells for an augmented T-helper 1 response</atitle><jtitle>Surgery</jtitle><addtitle>Surgery</addtitle><date>1998-08-01</date><risdate>1998</risdate><volume>124</volume><issue>2</issue><spage>269</spage><epage>277</epage><pages>269-277</pages><issn>0039-6060</issn><eissn>1532-7361</eissn><abstract>Background: The mechanisms responsible for altered T-cell responses and cytokine production after injury are not well understood. We used T-cell receptor (TCR) transgenic mice to study burn injury effects on naive versus antigen-activated CD4+ T cells in vivo.
Methods: One week after sham or burn injury, lymph node cells were prepared from TCR transgenic mice and stimulated with TCR transgene-specific antigens. T-cell proliferation was measured and culture supernatants were tested for interleukin-2 (IL-2), interferon-γ (IFN-γ), IL-4, and IL-10 by enzyme-linked immunosorbent assay (ELISA). Burn injury effects on antigen-activated T cells were studied by immunizing TCR transgenic or wild-type mice at the time of injury.
Results: The antigen-stimulated proliferation of naive CD4+ T cells was unaffected by burn injury and no increase in T-helper 2 (Th2)-type cytokine production was observed. Instead, burn injury augmented IFN-γ production by naive CD4+ transgenic T cells, and IL-2 production was marginally reduced. Thus, burn injury primed naive T cells for an enhanced Th1-type response. In contrast, antigen-specific proliferation, IL-2, and IFN-γ production by T cells harvested from immunized wild-type mice were suppressed. Unexpectedly, high mortality was observed when burn-injured TCR transgenic mice were immunized.
Conclusion: Our results show that burn injury has differential effects on naive and antigen-activated CD4+ T cells and can prime naive CD4+ T cells. (Surgery 1998;124:269-77.)</abstract><cop>United States</cop><pub>Mosby, Inc</pub><pmid>9706148</pmid><doi>10.1016/S0039-6060(98)70130-8</doi><tpages>9</tpages></addata></record> |
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subjects | Animals Antigen Presentation - immunology Antigens - immunology Burns - immunology Burns - metabolism CD4-Positive T-Lymphocytes - cytology CD4-Positive T-Lymphocytes - immunology CD4-Positive T-Lymphocytes - metabolism Cell Division - immunology Disease Models, Animal Interferon-gamma - biosynthesis Interleukin-10 - biosynthesis Interleukin-4 - biosynthesis Lymphocyte Activation - immunology Male Mice Mice, Inbred A Mice, Transgenic Ovalbumin - biosynthesis |
title | Burn injury primes naive CD4+ T cells for an augmented T-helper 1 response |
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