In the Absence of IL-12, CD4 + T Cell Responses to Intracellular Pathogens Fail to Default to a Th2 Pattern and Are Host Protective in an IL-10 −/− Setting
IL-12-deficient mice exposed to nonlethal infections with intracellular pathogens or repeatedly immunized with a pathogen extract developed lowered but nevertheless substantial numbers of IFN-γ + CD4 + T cells compared to those observed in wild-type animals. Moreover, the CD4 + responses in these kn...
Gespeichert in:
| Veröffentlicht in: | Immunity (Cambridge, Mass.) Mass.), 2002-03, Vol.16 (3), p.429-439 |
|---|---|
| Hauptverfasser: | , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 439 |
|---|---|
| container_issue | 3 |
| container_start_page | 429 |
| container_title | Immunity (Cambridge, Mass.) |
| container_volume | 16 |
| creator | Jankovic, Dragana Kullberg, Marika C. Hieny, Sara Caspar, Patricia Collazo, Carmen M. Sher, Alan |
| description | IL-12-deficient mice exposed to nonlethal infections with intracellular pathogens or repeatedly immunized with a pathogen extract developed lowered but nevertheless substantial numbers of IFN-γ
+ CD4
+ T cells compared to those observed in wild-type animals. Moreover, the CD4
+ responses in these knockout animals failed to default to a Th2 pattern. The protective efficacy of the Th1 cells developing in an IL-12-deficient setting was found to be limited by IL-10 since mice doubly deficient in IL-10 and IL-12 survived, while animals deficient in IL-12 alone succumbed to pathogen challenge. In contrast to IL-12 knockout mice, MyD88-deficient animals exposed to a Th1 microbial stimulus developed a pure Th2 response, arguing that this signaling element plays a more critical function than IL-12 in determining pathogen-induced CD4 polarization. |
| doi_str_mv | 10.1016/S1074-7613(02)00278-9 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_71533165</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S1074761302002789</els_id><sourcerecordid>3236375171</sourcerecordid><originalsourceid>FETCH-LOGICAL-c488t-b7db3602d5b2f53dc11893e884eba23cec224cfaba1651937832dc942ae70823</originalsourceid><addsrcrecordid>eNqFkc-KFDEQxhtR3HX1EZQCQRRtN3-6p9MnGWZdd2DAxZ17SKerd7L0JLNJesE38OwL-G4-icnMgODFQ0iR-lVV6vuK4iUlHymhs_MbSpqqbGaUvyXsHSGsEWX7qDilpG3KigryOMdH5KR4FsIdIbSqW_K0OKG0pVSw5rT4tbQQNwjzLqDVCG6A5aqk7AMsLip4D2tY4DjCNww7ZwMGiA6WNnql0_M0Kg_XKm7cLdoAl8qMOX-Bg5rGmEMF6w3LSERvQdke5h7hyoUI195F1NE8IJic2s8l8PvHz_N04AZjNPb2efFkUGPAF8f7rFhffl4vrsrV1y_LxXxV6kqIWHZN3_EZYX3dsaHmvU7rtRyFqLBTjGvUjFV6UJ2is5q2vBGc9bqtmMKGCMbPijeHtjvv7icMUW5NyCsqi24KsqE156k0ga__Ae_c5G36mqQ1ybrzukpUfaC0dyF4HOTOm63y3yUlMtsn9_bJ7I0kTO7tk22qe3XsPnVb7P9WHf1KwKcDgEmLB4NeBm2ycb3xSUzZO_OfEX8A7Oinxg</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1504180354</pqid></control><display><type>article</type><title>In the Absence of IL-12, CD4 + T Cell Responses to Intracellular Pathogens Fail to Default to a Th2 Pattern and Are Host Protective in an IL-10 −/− Setting</title><source>MEDLINE</source><source>Cell Press Free Archives</source><source>Access via ScienceDirect (Elsevier)</source><source>EZB-FREE-00999 freely available EZB journals</source><creator>Jankovic, Dragana ; Kullberg, Marika C. ; Hieny, Sara ; Caspar, Patricia ; Collazo, Carmen M. ; Sher, Alan</creator><creatorcontrib>Jankovic, Dragana ; Kullberg, Marika C. ; Hieny, Sara ; Caspar, Patricia ; Collazo, Carmen M. ; Sher, Alan</creatorcontrib><description>IL-12-deficient mice exposed to nonlethal infections with intracellular pathogens or repeatedly immunized with a pathogen extract developed lowered but nevertheless substantial numbers of IFN-γ
+ CD4
+ T cells compared to those observed in wild-type animals. Moreover, the CD4
+ responses in these knockout animals failed to default to a Th2 pattern. The protective efficacy of the Th1 cells developing in an IL-12-deficient setting was found to be limited by IL-10 since mice doubly deficient in IL-10 and IL-12 survived, while animals deficient in IL-12 alone succumbed to pathogen challenge. In contrast to IL-12 knockout mice, MyD88-deficient animals exposed to a Th1 microbial stimulus developed a pure Th2 response, arguing that this signaling element plays a more critical function than IL-12 in determining pathogen-induced CD4 polarization.</description><identifier>ISSN: 1074-7613</identifier><identifier>EISSN: 1097-4180</identifier><identifier>DOI: 10.1016/S1074-7613(02)00278-9</identifier><identifier>PMID: 11911827</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Adaptor Proteins, Signal Transducing ; Animals ; Antigens, Differentiation - genetics ; Antigens, Differentiation - immunology ; CD4-Positive T-Lymphocytes - immunology ; Hypotheses ; Immunity, Innate ; Interleukin-10 - genetics ; Interleukin-10 - immunology ; Interleukin-12 - genetics ; Interleukin-12 - immunology ; Lymphocytes ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Knockout ; Myeloid Differentiation Factor 88 ; Parasites ; Receptors, Immunologic - genetics ; Receptors, Immunologic - immunology ; Rodents ; Signal Transduction - immunology ; Spleen ; Th1 Cells - immunology ; Th2 Cells - immunology</subject><ispartof>Immunity (Cambridge, Mass.), 2002-03, Vol.16 (3), p.429-439</ispartof><rights>2002 Cell Press</rights><rights>Copyright Elsevier Limited Mar 2002</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c488t-b7db3602d5b2f53dc11893e884eba23cec224cfaba1651937832dc942ae70823</citedby><cites>FETCH-LOGICAL-c488t-b7db3602d5b2f53dc11893e884eba23cec224cfaba1651937832dc942ae70823</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S1074-7613(02)00278-9$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11911827$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jankovic, Dragana</creatorcontrib><creatorcontrib>Kullberg, Marika C.</creatorcontrib><creatorcontrib>Hieny, Sara</creatorcontrib><creatorcontrib>Caspar, Patricia</creatorcontrib><creatorcontrib>Collazo, Carmen M.</creatorcontrib><creatorcontrib>Sher, Alan</creatorcontrib><title>In the Absence of IL-12, CD4 + T Cell Responses to Intracellular Pathogens Fail to Default to a Th2 Pattern and Are Host Protective in an IL-10 −/− Setting</title><title>Immunity (Cambridge, Mass.)</title><addtitle>Immunity</addtitle><description>IL-12-deficient mice exposed to nonlethal infections with intracellular pathogens or repeatedly immunized with a pathogen extract developed lowered but nevertheless substantial numbers of IFN-γ
+ CD4
+ T cells compared to those observed in wild-type animals. Moreover, the CD4
+ responses in these knockout animals failed to default to a Th2 pattern. The protective efficacy of the Th1 cells developing in an IL-12-deficient setting was found to be limited by IL-10 since mice doubly deficient in IL-10 and IL-12 survived, while animals deficient in IL-12 alone succumbed to pathogen challenge. In contrast to IL-12 knockout mice, MyD88-deficient animals exposed to a Th1 microbial stimulus developed a pure Th2 response, arguing that this signaling element plays a more critical function than IL-12 in determining pathogen-induced CD4 polarization.</description><subject>Adaptor Proteins, Signal Transducing</subject><subject>Animals</subject><subject>Antigens, Differentiation - genetics</subject><subject>Antigens, Differentiation - immunology</subject><subject>CD4-Positive T-Lymphocytes - immunology</subject><subject>Hypotheses</subject><subject>Immunity, Innate</subject><subject>Interleukin-10 - genetics</subject><subject>Interleukin-10 - immunology</subject><subject>Interleukin-12 - genetics</subject><subject>Interleukin-12 - immunology</subject><subject>Lymphocytes</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Myeloid Differentiation Factor 88</subject><subject>Parasites</subject><subject>Receptors, Immunologic - genetics</subject><subject>Receptors, Immunologic - immunology</subject><subject>Rodents</subject><subject>Signal Transduction - immunology</subject><subject>Spleen</subject><subject>Th1 Cells - immunology</subject><subject>Th2 Cells - immunology</subject><issn>1074-7613</issn><issn>1097-4180</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc-KFDEQxhtR3HX1EZQCQRRtN3-6p9MnGWZdd2DAxZ17SKerd7L0JLNJesE38OwL-G4-icnMgODFQ0iR-lVV6vuK4iUlHymhs_MbSpqqbGaUvyXsHSGsEWX7qDilpG3KigryOMdH5KR4FsIdIbSqW_K0OKG0pVSw5rT4tbQQNwjzLqDVCG6A5aqk7AMsLip4D2tY4DjCNww7ZwMGiA6WNnql0_M0Kg_XKm7cLdoAl8qMOX-Bg5rGmEMF6w3LSERvQdke5h7hyoUI195F1NE8IJic2s8l8PvHz_N04AZjNPb2efFkUGPAF8f7rFhffl4vrsrV1y_LxXxV6kqIWHZN3_EZYX3dsaHmvU7rtRyFqLBTjGvUjFV6UJ2is5q2vBGc9bqtmMKGCMbPijeHtjvv7icMUW5NyCsqi24KsqE156k0ga__Ae_c5G36mqQ1ybrzukpUfaC0dyF4HOTOm63y3yUlMtsn9_bJ7I0kTO7tk22qe3XsPnVb7P9WHf1KwKcDgEmLB4NeBm2ycb3xSUzZO_OfEX8A7Oinxg</recordid><startdate>20020301</startdate><enddate>20020301</enddate><creator>Jankovic, Dragana</creator><creator>Kullberg, Marika C.</creator><creator>Hieny, Sara</creator><creator>Caspar, Patricia</creator><creator>Collazo, Carmen M.</creator><creator>Sher, Alan</creator><general>Elsevier Inc</general><general>Elsevier Limited</general><scope>6I.</scope><scope>AAFTH</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>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>NAPCQ</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20020301</creationdate><title>In the Absence of IL-12, CD4 + T Cell Responses to Intracellular Pathogens Fail to Default to a Th2 Pattern and Are Host Protective in an IL-10 −/− Setting</title><author>Jankovic, Dragana ; Kullberg, Marika C. ; Hieny, Sara ; Caspar, Patricia ; Collazo, Carmen M. ; Sher, Alan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c488t-b7db3602d5b2f53dc11893e884eba23cec224cfaba1651937832dc942ae70823</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Adaptor Proteins, Signal Transducing</topic><topic>Animals</topic><topic>Antigens, Differentiation - genetics</topic><topic>Antigens, Differentiation - immunology</topic><topic>CD4-Positive T-Lymphocytes - immunology</topic><topic>Hypotheses</topic><topic>Immunity, Innate</topic><topic>Interleukin-10 - genetics</topic><topic>Interleukin-10 - immunology</topic><topic>Interleukin-12 - genetics</topic><topic>Interleukin-12 - immunology</topic><topic>Lymphocytes</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Myeloid Differentiation Factor 88</topic><topic>Parasites</topic><topic>Receptors, Immunologic - genetics</topic><topic>Receptors, Immunologic - immunology</topic><topic>Rodents</topic><topic>Signal Transduction - immunology</topic><topic>Spleen</topic><topic>Th1 Cells - immunology</topic><topic>Th2 Cells - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jankovic, Dragana</creatorcontrib><creatorcontrib>Kullberg, Marika C.</creatorcontrib><creatorcontrib>Hieny, Sara</creatorcontrib><creatorcontrib>Caspar, Patricia</creatorcontrib><creatorcontrib>Collazo, Carmen M.</creatorcontrib><creatorcontrib>Sher, Alan</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Immunity (Cambridge, Mass.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jankovic, Dragana</au><au>Kullberg, Marika C.</au><au>Hieny, Sara</au><au>Caspar, Patricia</au><au>Collazo, Carmen M.</au><au>Sher, Alan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>In the Absence of IL-12, CD4 + T Cell Responses to Intracellular Pathogens Fail to Default to a Th2 Pattern and Are Host Protective in an IL-10 −/− Setting</atitle><jtitle>Immunity (Cambridge, Mass.)</jtitle><addtitle>Immunity</addtitle><date>2002-03-01</date><risdate>2002</risdate><volume>16</volume><issue>3</issue><spage>429</spage><epage>439</epage><pages>429-439</pages><issn>1074-7613</issn><eissn>1097-4180</eissn><abstract>IL-12-deficient mice exposed to nonlethal infections with intracellular pathogens or repeatedly immunized with a pathogen extract developed lowered but nevertheless substantial numbers of IFN-γ
+ CD4
+ T cells compared to those observed in wild-type animals. Moreover, the CD4
+ responses in these knockout animals failed to default to a Th2 pattern. The protective efficacy of the Th1 cells developing in an IL-12-deficient setting was found to be limited by IL-10 since mice doubly deficient in IL-10 and IL-12 survived, while animals deficient in IL-12 alone succumbed to pathogen challenge. In contrast to IL-12 knockout mice, MyD88-deficient animals exposed to a Th1 microbial stimulus developed a pure Th2 response, arguing that this signaling element plays a more critical function than IL-12 in determining pathogen-induced CD4 polarization.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>11911827</pmid><doi>10.1016/S1074-7613(02)00278-9</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1074-7613 |
| ispartof | Immunity (Cambridge, Mass.), 2002-03, Vol.16 (3), p.429-439 |
| issn | 1074-7613 1097-4180 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_71533165 |
| source | MEDLINE; Cell Press Free Archives; Access via ScienceDirect (Elsevier); EZB-FREE-00999 freely available EZB journals |
| subjects | Adaptor Proteins, Signal Transducing Animals Antigens, Differentiation - genetics Antigens, Differentiation - immunology CD4-Positive T-Lymphocytes - immunology Hypotheses Immunity, Innate Interleukin-10 - genetics Interleukin-10 - immunology Interleukin-12 - genetics Interleukin-12 - immunology Lymphocytes Mice Mice, Inbred BALB C Mice, Inbred C57BL Mice, Knockout Myeloid Differentiation Factor 88 Parasites Receptors, Immunologic - genetics Receptors, Immunologic - immunology Rodents Signal Transduction - immunology Spleen Th1 Cells - immunology Th2 Cells - immunology |
| title | In the Absence of IL-12, CD4 + T Cell Responses to Intracellular Pathogens Fail to Default to a Th2 Pattern and Are Host Protective in an IL-10 −/− Setting |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-02T18%3A59%3A02IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=In%20the%20Absence%20of%20IL-12,%20CD4%20+%20T%20Cell%20Responses%20to%20Intracellular%20Pathogens%20Fail%20to%20Default%20to%20a%20Th2%20Pattern%20and%20Are%20Host%20Protective%20in%20an%20IL-10%20%E2%88%92/%E2%88%92%20Setting&rft.jtitle=Immunity%20(Cambridge,%20Mass.)&rft.au=Jankovic,%20Dragana&rft.date=2002-03-01&rft.volume=16&rft.issue=3&rft.spage=429&rft.epage=439&rft.pages=429-439&rft.issn=1074-7613&rft.eissn=1097-4180&rft_id=info:doi/10.1016/S1074-7613(02)00278-9&rft_dat=%3Cproquest_cross%3E3236375171%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1504180354&rft_id=info:pmid/11911827&rft_els_id=S1074761302002789&rfr_iscdi=true |