Document Detail

The role of B cells in the development of CD4 effector T cells during a polarized Th2 immune response.
MedLine Citation:
PMID:  17785819     Owner:  NLM     Status:  MEDLINE    
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.
Qian Liu; Zhugong Liu; Cristina T Rozo; Hossein A Hamed; Farhang Alem; Joseph F Urban; William C Gause
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  179     ISSN:  0022-1767     ISO Abbreviation:  J. Immunol.     Publication Date:  2007 Sep 
Date Detail:
Created Date:  2007-09-05     Completed Date:  2007-11-05     Revised Date:  2014-09-10    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  3821-30     Citation Subset:  AIM; IM    
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MeSH Terms
Adoptive Transfer
Amino Acid Sequence
B-Lymphocytes / immunology*,  parasitology,  pathology,  transplantation
CD4-Positive T-Lymphocytes / cytology*,  immunology*,  parasitology,  transplantation
Cell Differentiation / genetics,  immunology*
Epitopes, T-Lymphocyte / immunology
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
AI31678/AI/NIAID NIH HHS; R01 AI031678/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/AI/NIAID NIH HHS; R01 AI066188-01A1/AI/NIAID NIH HHS; R01 AI066188-02/AI/NIAID NIH HHS
Reg. No./Substance:
0/Epitopes, T-Lymphocyte; 0/OVA 323-339; 0/Peptide Fragments; 9006-59-1/Ovalbumin

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