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Antigen-specific and non-specific CD4 + T cell recruitment and proliferation during influenza infection
To track epitope-specific CD4 + T cells at a single-cell level during influenza infection, the MHC class II-restricted OVA 323–339 epitope was engineered into the neuraminidase stalk of influenza/A/WSN, creating a surrogate viral antigen. The recombinant virus, influenza A/WSN/OVA II, replicated wel...
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| Published in: | Virology (New York, N.Y.) N.Y.), 2005-09, Vol.340 (2), p.296-306 |
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| cites | cdi_FETCH-LOGICAL-c454t-a5744960ce31e1c04ea7b2d52b06d2c9b1dd030e1aeacd381e90d0cfc62843fb3 |
| container_end_page | 306 |
| container_issue | 2 |
| container_start_page | 296 |
| container_title | Virology (New York, N.Y.) |
| container_volume | 340 |
| creator | Chapman, Timothy J. Castrucci, Maria R. Padrick, Ryan C. Bradley, Linda M. Topham, David J. |
| description | To track epitope-specific CD4
+ T cells at a single-cell level during influenza infection, the MHC class II-restricted OVA
323–339 epitope was engineered into the neuraminidase stalk of influenza/A/WSN, creating a surrogate viral antigen. The recombinant virus, influenza A/WSN/OVA
II, replicated well, was cleared normally, and stimulated both wild-type and DO11.10 or OT-II TCR transgenic OVA-specific CD4
+ T cells. OVA-specific CD4 T cells proliferated during infection only when the OVA epitope was present. However, previously primed (but not naive) transgenic CD4
+ T cells were recruited to the infected lung both in the presence and absence of the OVA
323–339 epitope. These data show that, when primed, CD4
+ T cells may traffic to the lung in the absence of antigen, but do not proliferate. These results also document a useful tool for the study of CD4 T cells in influenza infection. |
| doi_str_mv | 10.1016/j.virol.2005.06.023 |
| format | article |
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323–339 epitope was engineered into the neuraminidase stalk of influenza/A/WSN, creating a surrogate viral antigen. The recombinant virus, influenza A/WSN/OVA
II, replicated well, was cleared normally, and stimulated both wild-type and DO11.10 or OT-II TCR transgenic OVA-specific CD4
+ T cells. OVA-specific CD4 T cells proliferated during infection only when the OVA epitope was present. However, previously primed (but not naive) transgenic CD4
+ T cells were recruited to the infected lung both in the presence and absence of the OVA
323–339 epitope. These data show that, when primed, CD4
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+ T cells at a single-cell level during influenza infection, the MHC class II-restricted OVA
323–339 epitope was engineered into the neuraminidase stalk of influenza/A/WSN, creating a surrogate viral antigen. The recombinant virus, influenza A/WSN/OVA
II, replicated well, was cleared normally, and stimulated both wild-type and DO11.10 or OT-II TCR transgenic OVA-specific CD4
+ T cells. OVA-specific CD4 T cells proliferated during infection only when the OVA epitope was present. However, previously primed (but not naive) transgenic CD4
+ T cells were recruited to the infected lung both in the presence and absence of the OVA
323–339 epitope. These data show that, when primed, CD4
+ T cells may traffic to the lung in the absence of antigen, but do not proliferate. These results also document a useful tool for the study of CD4 T cells in influenza infection.</description><subject>60 APPLIED LIFE SCIENCES</subject><subject>Adoptive Transfer</subject><subject>Amino Acid Sequence</subject><subject>amino acid sequences</subject><subject>Animals</subject><subject>Antigen</subject><subject>ANTIGENS</subject><subject>CD4 + T cell</subject><subject>CD4-positive T-lymphocytes</subject><subject>CD4-Positive T-Lymphocytes - immunology</subject><subject>Cell Line</subject><subject>CELL PROLIFERATION</subject><subject>cell-mediated immunity</subject><subject>Disease Models, Animal</subject><subject>Dogs</subject><subject>human health</subject><subject>INFLUENZA</subject><subject>Influenza A virus</subject><subject>Influenza A virus - isolation & purification</subject><subject>Kidney</subject><subject>LUNGS</subject><subject>Lymphocyte Activation</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Transgenic</subject><subject>Molecular Sequence Data</subject><subject>Orthomyxoviridae Infections - immunology</subject><subject>OVA</subject><subject>Ovalbumin - chemistry</subject><subject>Peptide Fragments</subject><subject>viral antigens</subject><subject>Viral Plaque Assay</subject><subject>VIRUSES</subject><issn>0042-6822</issn><issn>1096-0341</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><recordid>eNp9kU1v1DAQhi0EokvhFyBBJCQuKGH8ESc59FAtH61UqQfas-XYk8WrrL3YSSX49TjNSnDqyfb4mdH7zkvIWwoVBSo_76sHF8NYMYC6AlkB48_IhkInS-CCPicbAMFK2TJ2Rl6ltIf8bhp4Sc6ohFrQtt2Q3aWf3A59mY5o3OBMob0tfPivsP0iik_FXWFwHIuIJs5uOqCfHsljVuAGjHpywRd2js7vCueHcUb_Ry83NMvXa_Ji0GPCN6fznNx_-3q3vSpvbr9fby9vSiNqMZW6boToJBjkFKkBgbrpma1ZD9Iy0_XUWuCAVKM2lrcUO7BgBiNZK_jQ83PyYZ0b0uRUMm5C89ME77MMxaBhHeV1pj6uVJb_a8Y0qYNLiz_tMcxJyVYCrWmTQb6CJoaUIg7qGN1Bx9-KglpSUHv1mIJaUlAgVU4hd707jZ_7A9p_Pae1Z-D9Cgw6KL2LLqn7HwwoBwoN1Exm4mIlMC_rwWFcvKA3aF1crNjgnpTwFxKfo0g</recordid><startdate>20050930</startdate><enddate>20050930</enddate><creator>Chapman, Timothy J.</creator><creator>Castrucci, Maria R.</creator><creator>Padrick, Ryan C.</creator><creator>Bradley, Linda M.</creator><creator>Topham, David J.</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</scope><scope>FBQ</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>7X8</scope><scope>OTOTI</scope></search><sort><creationdate>20050930</creationdate><title>Antigen-specific and non-specific CD4 + T cell recruitment and proliferation during influenza infection</title><author>Chapman, Timothy J. ; 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+ T cells at a single-cell level during influenza infection, the MHC class II-restricted OVA
323–339 epitope was engineered into the neuraminidase stalk of influenza/A/WSN, creating a surrogate viral antigen. The recombinant virus, influenza A/WSN/OVA
II, replicated well, was cleared normally, and stimulated both wild-type and DO11.10 or OT-II TCR transgenic OVA-specific CD4
+ T cells. OVA-specific CD4 T cells proliferated during infection only when the OVA epitope was present. However, previously primed (but not naive) transgenic CD4
+ T cells were recruited to the infected lung both in the presence and absence of the OVA
323–339 epitope. These data show that, when primed, CD4
+ T cells may traffic to the lung in the absence of antigen, but do not proliferate. These results also document a useful tool for the study of CD4 T cells in influenza infection.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>16054188</pmid><doi>10.1016/j.virol.2005.06.023</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Virology (New York, N.Y.), 2005-09, Vol.340 (2), p.296-306 |
| issn | 0042-6822 1096-0341 |
| language | eng |
| recordid | cdi_osti_scitechconnect_20729135 |
| source | BACON - Elsevier - GLOBAL_SCIENCEDIRECT-OPENACCESS; ScienceDirect Journals |
| subjects | 60 APPLIED LIFE SCIENCES Adoptive Transfer Amino Acid Sequence amino acid sequences Animals Antigen ANTIGENS CD4 + T cell CD4-positive T-lymphocytes CD4-Positive T-Lymphocytes - immunology Cell Line CELL PROLIFERATION cell-mediated immunity Disease Models, Animal Dogs human health INFLUENZA Influenza A virus Influenza A virus - isolation & purification Kidney LUNGS Lymphocyte Activation Mice Mice, Inbred C57BL Mice, Transgenic Molecular Sequence Data Orthomyxoviridae Infections - immunology OVA Ovalbumin - chemistry Peptide Fragments viral antigens Viral Plaque Assay VIRUSES |
| title | Antigen-specific and non-specific CD4 + T cell recruitment and proliferation during influenza infection |
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