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IL-10 Is Required for Optimal CD8 T Cell Memory following Listeria monocytogenes Infection
IL-10 is an important immunoregulatory cytokine that plays a central role in maintaining a balance between protective immunity against infection and limiting proinflammatory responses to self or cross-reactive Ags. We examined the full effects of IL-10 deficiency on the establishment and quality of...
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Published in: | Journal of Immunology 2006-08, Vol.177 (4), p.2565-2574 |
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creator | Foulds, Kathryn E Rotte, Masashi J Seder, Robert A |
description | IL-10 is an important immunoregulatory cytokine that plays a central role in maintaining a balance between protective immunity against infection and limiting proinflammatory responses to self or cross-reactive Ags. We examined the full effects of IL-10 deficiency on the establishment and quality of T cell memory using murine listeriosis as a model system. IL-10(-/-) mice had reduced bacterial loads and a shorter duration of primary infection than did wild-type mice. However, the number of Ag-specific T cells in secondary lymphoid and nonlymphoid organs was diminished in IL-10(-/-) mice, compared with wild-type mice, at the peak of the effector response. Moreover, the frequency and protective capacity of memory T cells also were reduced in IL-10(-/-) mice when assessed up to 100 days postinfection. Remarkably, this effect was more pronounced for CD8 T cells than CD4 T cells. To address whether differences in the number of bacteria and duration of primary infection could explain these findings, both strains of mice were treated with ampicillin 24 hours after primary infection. Despite there being more comparable bacterial loads during primary infection, IL-10(-/-) mice still generated fewer memory CD8 T cells and were less protected against secondary infection than were wild-type mice. Finally, the adoptive transfer of purified CD8 T cells from previously infected wild-type mice into naive recipients conferred better protection than the transfer of CD8 T cells from immune IL-10(-/-) mice. Overall, these data show that IL-10 plays an unexpected role in promoting and/or sustaining CD8 T cell memory following Listeria monocytogenes infection. |
doi_str_mv | 10.4049/jimmunol.177.4.2565 |
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We examined the full effects of IL-10 deficiency on the establishment and quality of T cell memory using murine listeriosis as a model system. IL-10(-/-) mice had reduced bacterial loads and a shorter duration of primary infection than did wild-type mice. However, the number of Ag-specific T cells in secondary lymphoid and nonlymphoid organs was diminished in IL-10(-/-) mice, compared with wild-type mice, at the peak of the effector response. Moreover, the frequency and protective capacity of memory T cells also were reduced in IL-10(-/-) mice when assessed up to 100 days postinfection. Remarkably, this effect was more pronounced for CD8 T cells than CD4 T cells. To address whether differences in the number of bacteria and duration of primary infection could explain these findings, both strains of mice were treated with ampicillin 24 hours after primary infection. Despite there being more comparable bacterial loads during primary infection, IL-10(-/-) mice still generated fewer memory CD8 T cells and were less protected against secondary infection than were wild-type mice. Finally, the adoptive transfer of purified CD8 T cells from previously infected wild-type mice into naive recipients conferred better protection than the transfer of CD8 T cells from immune IL-10(-/-) mice. 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We examined the full effects of IL-10 deficiency on the establishment and quality of T cell memory using murine listeriosis as a model system. IL-10(-/-) mice had reduced bacterial loads and a shorter duration of primary infection than did wild-type mice. However, the number of Ag-specific T cells in secondary lymphoid and nonlymphoid organs was diminished in IL-10(-/-) mice, compared with wild-type mice, at the peak of the effector response. Moreover, the frequency and protective capacity of memory T cells also were reduced in IL-10(-/-) mice when assessed up to 100 days postinfection. Remarkably, this effect was more pronounced for CD8 T cells than CD4 T cells. To address whether differences in the number of bacteria and duration of primary infection could explain these findings, both strains of mice were treated with ampicillin 24 hours after primary infection. Despite there being more comparable bacterial loads during primary infection, IL-10(-/-) mice still generated fewer memory CD8 T cells and were less protected against secondary infection than were wild-type mice. Finally, the adoptive transfer of purified CD8 T cells from previously infected wild-type mice into naive recipients conferred better protection than the transfer of CD8 T cells from immune IL-10(-/-) mice. Overall, these data show that IL-10 plays an unexpected role in promoting and/or sustaining CD8 T cell memory following Listeria monocytogenes infection.</description><subject>Adoptive Transfer</subject><subject>Animals</subject><subject>CD8-Positive T-Lymphocytes - immunology</subject><subject>CD8-Positive T-Lymphocytes - microbiology</subject><subject>CD8-Positive T-Lymphocytes - transplantation</subject><subject>Female</subject><subject>Immunologic Memory - genetics</subject><subject>Interleukin-10 - deficiency</subject><subject>Interleukin-10 - genetics</subject><subject>Interleukin-10 - physiology</subject><subject>Listeria monocytogenes</subject><subject>Listeriosis - genetics</subject><subject>Listeriosis - immunology</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><issn>0022-1767</issn><issn>1550-6606</issn><issn>1365-2567</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><recordid>eNqFkE1L7DAUhoMoOn78AuGSla46Jml70i4v49fAiCC6cRPSzOkYaZsxaSnz743MiO5cHQ7neV8ODyHnnE0zlpVX77Zth841Uy7lNJuKHPI9MuF5zhIABvtkwpgQCZcgj8hxCO-MMWAiOyRHHIqiYLyYkNf5IuGMzgN9wo_BelzS2nn6uO5tqxs6uy7oM51h09AHbJ3fxGvTuNF2K7qwoUdvNW1d58ymdyvsMNB5V6PpretOyUGtm4Bnu3lCXm5vnmf3yeLxbj77v0hMCtAnRgo0BiUHyDVgzkvDq4qlsihLJmqoNFS41AXEXeSlzirQCAJLEKJOyzw9IRfb3rV3HwOGXrU2mPiy7tANQUEhhWAS_gR5mcoUMhHBdAsa70LwWKu1jzr8RnGmvtyrb_cquleZ-nIfU_929UPV4vIns5Mdgcst8GZXb2N0rUJ03EScq3Ecf1V9AtTQjp8</recordid><startdate>20060815</startdate><enddate>20060815</enddate><creator>Foulds, Kathryn E</creator><creator>Rotte, Masashi J</creator><creator>Seder, Robert A</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>7QL</scope><scope>7T5</scope><scope>C1K</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20060815</creationdate><title>IL-10 Is Required for Optimal CD8 T Cell Memory following Listeria monocytogenes Infection</title><author>Foulds, Kathryn E ; Rotte, Masashi J ; Seder, Robert A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c366t-c72ecce71665a6e519c1bb03789902f6ba6beda86899259a4b6ae62e9622f3953</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Adoptive Transfer</topic><topic>Animals</topic><topic>CD8-Positive T-Lymphocytes - immunology</topic><topic>CD8-Positive T-Lymphocytes - microbiology</topic><topic>CD8-Positive T-Lymphocytes - transplantation</topic><topic>Female</topic><topic>Immunologic Memory - genetics</topic><topic>Interleukin-10 - deficiency</topic><topic>Interleukin-10 - genetics</topic><topic>Interleukin-10 - physiology</topic><topic>Listeria monocytogenes</topic><topic>Listeriosis - genetics</topic><topic>Listeriosis - immunology</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Foulds, Kathryn E</creatorcontrib><creatorcontrib>Rotte, Masashi J</creatorcontrib><creatorcontrib>Seder, Robert 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>Bacteriology Abstracts (Microbiology B)</collection><collection>Immunology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of Immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Foulds, Kathryn E</au><au>Rotte, Masashi J</au><au>Seder, Robert A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>IL-10 Is Required for Optimal CD8 T Cell Memory following Listeria monocytogenes Infection</atitle><jtitle>Journal of Immunology</jtitle><addtitle>J Immunol</addtitle><date>2006-08-15</date><risdate>2006</risdate><volume>177</volume><issue>4</issue><spage>2565</spage><epage>2574</epage><pages>2565-2574</pages><issn>0022-1767</issn><eissn>1550-6606</eissn><eissn>1365-2567</eissn><abstract>IL-10 is an important immunoregulatory cytokine that plays a central role in maintaining a balance between protective immunity against infection and limiting proinflammatory responses to self or cross-reactive Ags. We examined the full effects of IL-10 deficiency on the establishment and quality of T cell memory using murine listeriosis as a model system. IL-10(-/-) mice had reduced bacterial loads and a shorter duration of primary infection than did wild-type mice. However, the number of Ag-specific T cells in secondary lymphoid and nonlymphoid organs was diminished in IL-10(-/-) mice, compared with wild-type mice, at the peak of the effector response. Moreover, the frequency and protective capacity of memory T cells also were reduced in IL-10(-/-) mice when assessed up to 100 days postinfection. Remarkably, this effect was more pronounced for CD8 T cells than CD4 T cells. To address whether differences in the number of bacteria and duration of primary infection could explain these findings, both strains of mice were treated with ampicillin 24 hours after primary infection. Despite there being more comparable bacterial loads during primary infection, IL-10(-/-) mice still generated fewer memory CD8 T cells and were less protected against secondary infection than were wild-type mice. Finally, the adoptive transfer of purified CD8 T cells from previously infected wild-type mice into naive recipients conferred better protection than the transfer of CD8 T cells from immune IL-10(-/-) mice. Overall, these data show that IL-10 plays an unexpected role in promoting and/or sustaining CD8 T cell memory following Listeria monocytogenes infection.</abstract><cop>United States</cop><pub>Am Assoc Immnol</pub><pmid>16888018</pmid><doi>10.4049/jimmunol.177.4.2565</doi><tpages>10</tpages></addata></record> |
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subjects | Adoptive Transfer Animals CD8-Positive T-Lymphocytes - immunology CD8-Positive T-Lymphocytes - microbiology CD8-Positive T-Lymphocytes - transplantation Female Immunologic Memory - genetics Interleukin-10 - deficiency Interleukin-10 - genetics Interleukin-10 - physiology Listeria monocytogenes Listeriosis - genetics Listeriosis - immunology Mice Mice, Inbred C57BL Mice, Knockout |
title | IL-10 Is Required for Optimal CD8 T Cell Memory following Listeria monocytogenes Infection |
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