| The role of B cells in the development of CD4 effector T cells during a polarized Th2 immune response. | |
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MedLine Citation:
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PMID: 17785819 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Previous studies have suggested that B cells promote Th2 cell development by inhibiting Th1 cell differentiation. To examine whether B cells are directly required for the development of IL-4-producing T cells in the lymph node during a highly polarized Th2 response, B cell-deficient and wild-type mice were inoculated with the nematode parasite, Nippostrongylus brasiliensis. On day 7, in the absence of increased IFN-gamma, IL-4 protein and gene expression from CD4 T cells in the draining lymph nodes were markedly reduced in B cell-deficient mice and could not be restored by multiple immunizations. Using a DO11.10 T cell adoptive transfer system, OVA-specific T cell IL-4 production and cell cycle progression, but not cell surface expression of early activation markers, were impaired in B cell-deficient recipient mice following immunization with N. brasiliensis plus OVA. Laser capture microdissection and immunofluorescent staining showed that pronounced IL-4 mRNA and protein secretion by donor DO11.10 T cells first occurred in the T cell:B cell zone of the lymph node shortly after inoculation of IL-4-/- recipients, suggesting that this microenvironment is critical for initial Th2 cell development. Reconstitution of B cell-deficient mice with wild-type naive B cells, or IL-4-/- B cells, substantially restored Ag-specific T cell IL-4 production. However, reconstitution with B7-1/B7-2-deficient B cells failed to rescue the IL-4-producing DO11.10 T cells. These results suggest that B cells, expressing B7 costimulatory molecules, are required in the absence of an underlying IFN-gamma-mediated response for the development of a polarized primary Ag-specific Th2 response in vivo. |
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Authors:
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Qian Liu; Zhugong Liu; Cristina T Rozo; Hossein A Hamed; Farhang Alem; Joseph F Urban; William C Gause |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural |
Journal Detail:
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Title: Journal of immunology (Baltimore, Md. : 1950) Volume: 179 ISSN: 0022-1767 ISO Abbreviation: J. Immunol. Publication Date: 2007 Sep |
Date Detail:
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Created Date: 2007-09-05 Completed Date: 2007-11-05 Revised Date: 2011-04-28 |
Medline Journal Info:
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Nlm Unique ID: 2985117R Medline TA: J Immunol Country: United States |
Other Details:
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Languages: eng Pagination: 3821-30 Citation Subset: AIM; IM |
Affiliation:
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Department of Medicine, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, Newark, NJ 07103, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adoptive Transfer Amino Acid Sequence Animals B-Lymphocytes / immunology*, parasitology, pathology, transplantation CD4-Positive T-Lymphocytes / cytology*, immunology*, parasitology, transplantation Cell Differentiation / genetics, immunology* Epitopes, T-Lymphocyte / immunology Mice Mice, Inbred BALB C Mice, Mutant Strains Mice, Transgenic Molecular Sequence Data Nippostrongylus / immunology Ovalbumin / administration & dosage, immunology Peptide Fragments / administration & dosage, immunology Strongylida Infections / genetics, immunology, metabolism Th2 Cells / immunology*, metabolism*, parasitology, pathology |
| Grant Support | |
ID/Acronym/Agency:
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AI31678/AI/NIAID NIH HHS; R01 AI031678-10/AI/NIAID NIH HHS; R01 AI031678-11/AI/NIAID NIH HHS; R01 AI031678-12/AI/NIAID NIH HHS; R01 AI031678-13/AI/NIAID NIH HHS; R01 AI031678-14/AI/NIAID NIH HHS; R01 AI066188-01A1/AI/NIAID NIH HHS; R01 AI066188-02/AI/NIAID NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Epitopes, T-Lymphocyte; 0/OVA 323-339; 0/Peptide Fragments; 9006-59-1/Ovalbumin |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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