Document Detail

Interleukin-4-dependent innate collaboration between iNKT cells and B-1 B cells controls adaptative contact sensitivity.
MedLine Citation:
PMID:  16556268     Owner:  NLM     Status:  MEDLINE    
We showed that hepatic Valpha14+ invariant natural killer T (iNKT) cells, via their rapid interleukin (IL)-4 production, activate B-1 cells to initiate contact sensitivity (CS). This innate collaboration was absent in IL-4(-/-) and signal transducer and activator of transcription (STAT)-6(-/-) mice and was inhibited by anti-IL-4 treatment. These mice have defective CS because they fail to locally recruit the sensitized effector T cells of acquired immunity. Their CS is reconstituted by transfer of downstream-acting 1-day immune B-1 cells from wild-type mice. Responses were not reconstituted with B-1 cells from IL-4 receptor-alpha(-/-) or STAT-6(-/-) mice, nor by IL-4 treatment of B cell-deficient mice at immunization. Finally, IL-4 was preferentially and transiently produced by hepatic iNKT cells within 7 min after sensitization to mediate collaboration between innate-like iNKT cells and the B-1 B cells that participate in the recruitment of effector T cells in vivo.
Regis A Campos; Marian Szczepanik; Atsuko Itakura; Mariette Lisbonne; Neelendu Dey; Maria C Leite-de-Moraes; Philip W Askenase
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Immunology     Volume:  117     ISSN:  0019-2805     ISO Abbreviation:  Immunology     Publication Date:  2006 Apr 
Date Detail:
Created Date:  2006-03-24     Completed Date:  2006-05-03     Revised Date:  2013-06-07    
Medline Journal Info:
Nlm Unique ID:  0374672     Medline TA:  Immunology     Country:  England    
Other Details:
Languages:  eng     Pagination:  536-47     Citation Subset:  IM    
Section of Allergy and Clinical Immunology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520-8013, USA.
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MeSH Terms
Adoptive Transfer
Antigens, Differentiation, B-Lymphocyte / analysis
B-Lymphocyte Subsets / immunology*
Cell Communication / immunology
Dermatitis, Contact / etiology,  immunology*
Flow Cytometry
Histocompatibility Antigens Class II / analysis
Immune Tolerance / immunology
Interleukin-4 / biosynthesis,  immunology*
Killer Cells, Natural / immunology*
Liver / immunology
Lymphocyte Activation / immunology
Mice, Inbred BALB C
Mice, Inbred CBA
Picryl Chloride
Receptors, Antigen, T-Cell, alpha-beta / analysis
Receptors, Interleukin-4 / immunology
STAT6 Transcription Factor / immunology
T-Lymphocyte Subsets / immunology*
Grant Support
Reg. No./Substance:
0/Antigens, Differentiation, B-Lymphocyte; 0/Histocompatibility Antigens Class II; 0/Receptors, Antigen, T-Cell, alpha-beta; 0/Receptors, Interleukin-4; 0/STAT6 Transcription Factor; 0/Stat6 protein, mouse; 0/invariant chain; 207137-56-2/Interleukin-4; 88-88-0/Picryl Chloride

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