Document Detail


CCR2 plays a critical role in dendritic cell maturation: possible role of CCL2 and NF-kappa B.
MedLine Citation:
PMID:  20404272     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We postulated that CCR2-driven activation of the transcription factor NF-kappaB plays a critical role in dendritic cell (DC) maturation (e.g., migration, costimulation, and IL-12p70 production), necessary for the generation of protective immune responses against the intracellular pathogen Leishmania major. Supporting this notion, we found that CCR2, its ligand CCL2, and NF-kappaB were required for CCL19 production and adequate Langerhans cell (LC) migration both ex vivo and in vivo. Furthermore, a role for CCR2 in upregulating costimulatory molecules was indicated by the reduced expression of CD80, CD86, and CD40 in Ccr2(-/-) bone marrow-derived dendritic cells (BMDCs) compared with wild-type (WT) BMDCs. Four lines of evidence suggested that CCR2 plays a critical role in the induction of protective immunity against L. major by regulating IL-12p70 production and migration of DC populations such as LCs. First, compared with WT, Ccr2(-/-) lymph node cells, splenocytes, BMDCs, and LCs produced lower levels of IL-12p70 following stimulation with LPS/IFN-gamma or L. major. Second, a reduced number of LCs carried L. major from the skin to the draining lymph nodes in Ccr2(-/-) mice compared with WT mice. Third, early treatment with exogenous IL-12 reversed the susceptibility to L. major infection in Ccr2(-/-) mice. Finally, disruption of IL-12p70 in radioresistant cells, such as LCs, but not in BMDCs resulted in the inability to mount a fully protective immune response in bone marrow chimeric mice. Collectively, our data point to an important role for CCR2-driven activation of NF-kappaB in the regulation of DC/LC maturation processes that regulate protective immunity against intracellular pathogens.
Authors:
Fabio Jimenez; Marlon P Quinones; Hernan G Martinez; Carlos A Estrada; Kassandra Clark; Edgar Garavito; Jessica Ibarra; Peter C Melby; Seema S Ahuja
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2010-04-19
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  184     ISSN:  1550-6606     ISO Abbreviation:  J. Immunol.     Publication Date:  2010 May 
Date Detail:
Created Date:  2010-05-20     Completed Date:  2010-07-19     Revised Date:  2011-09-26    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  5571-81     Citation Subset:  AIM; IM    
Affiliation:
Audie L. Murphy Division, Veterans Administration Center for Research on AIDS and HIV-1 Infection, South Texas Veterans Health Care System, San Antonio, TX 78229, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Differentiation / genetics,  immunology*
Cell Movement / genetics,  immunology
Cells, Cultured
Chemokine CCL2 / deficiency,  genetics,  physiology*
Dendritic Cells / immunology*,  metabolism*,  pathology
Interleukin-12 / biosynthesis,  genetics
Langerhans Cells / immunology,  metabolism,  pathology
Leishmania major / immunology
Leishmaniasis, Cutaneous / immunology,  metabolism,  pathology
Mice
Mice, Inbred C57BL
Mice, Knockout
Mice, SCID
Models, Immunological
NF-kappa B / metabolism,  physiology*
Receptors, CCR2 / biosynthesis,  deficiency,  physiology*
Transcriptional Activation / immunology
Up-Regulation / genetics,  immunology
Grant Support
ID/Acronym/Agency:
R01 AI048644-01A1/AI/NIAID NIH HHS; R01 AR052755-01A2/AR/NIAMS NIH HHS; R01-AI48644/AI/NIAID NIH HHS; R01-AR052755/AR/NIAMS NIH HHS
Chemical
Reg. No./Substance:
0/Ccl2 protein, mouse; 0/Ccr2 protein, mouse; 0/Chemokine CCL2; 0/NF-kappa B; 0/Receptors, CCR2; 187348-17-0/Interleukin-12

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