PMID- 14759987
OWN - NLM
STAT- MEDLINE
DCOM- 20040227
LR  - 20220310
IS  - 1460-2105 (Electronic)
IS  - 0027-8874 (Linking)
VI  - 96
IP  - 3
DP  - 2004 Feb 4
TI  - Mobilization of dendritic cell precursors into the circulation by administration 
      of MIP-1alpha in mice.
PG  - 201-9
AB  - BACKGROUND: Dendritic cells (DCs) play a central role in immune responses and may 
      be useful adjuvants for tumor vaccine therapy. We previously reported that 
      F4/80(-)B220(-)CD11c(+) DC precursors expressing the CC chemokine receptors CCR1 
      and CCR5 are mobilized rapidly into the circulation in mice injected with 
      Propionibacterium acnes and are recruited into inflammatory tissue by macrophage 
      inflammatory protein 1alpha (MIP-1alpha), which binds to CCR1 and CCR5. Here we 
      investigate the mechanisms of DC precursor mobilization and the antitumor effect 
      of these cells in mice. METHODS: Numbers of DC precursors in peripheral blood 
      were determined in P. acnes-treated mice (groups of 10 C57BL/B6 [B6] wild-type 
      mice, CCR1(-/-) mice, CCR5(-/-) mice, and B6 mice treated with antibody to 
      MIP-1alpha or control antibody) and in B6 mice injected with recombinant 
      MIP-1alpha. MIP-1alpha-mobilized DC precursors matured by treatment with 
      granulocyte-macrophage colony-stimulating factor, interleukin 4, and tumor 
      necrosis factor-alpha and pulsed with B16 melanoma lysates were assayed for their 
      ability to confer protective immunity against tumor challenge in vivo and to 
      induce cytotoxic T lymphocytes against B16 tumor cells in vitro. RESULTS: The 
      recruitment of DC precursors into the circulation by P. acnes administration was 
      higher in B6 mice (12.6%, 95% confidence interval [CI] = 9.1% to 16.1%) than in 
      CCR1(-/-) (9.0%, 95% CI = 7.5% to 10.5%), CCR5(-/-) (6.3%, 95% CI = 5.2% to 
      7.3%), or anti-MIP-1alpha antibody-treated (6.6%, 95% CI = 5.7% to 7.5%) mice. 
      Injection of MIP-1alpha also mobilized DC precursors into the circulation (13.1%, 
      95% CI = 10.8% to 15.6%). Matured MIP-1alpha-mobilized-DC precursors pulsed with 
      B16 tumor lysates elicited B16-specific antitumor immunity in vitro and in vivo. 
      CONCLUSIONS: MIP-1alpha and its receptors are important in recruiting DC 
      precursors into the circulation. DC precursors mobilized rapidly by MIP-1alpha 
      may provide sufficient useful DC precursors for DC-based vaccination in cancer 
      treatment.
FAU - Zhang, Yanyun
AU  - Zhang Y
AD  - Department of Molecular Preventive Medicine, School of Medicine, The University 
      of Tokyo, Tokyo, Japan.
FAU - Yoneyama, Hiroyuki
AU  - Yoneyama H
FAU - Wang, Yong
AU  - Wang Y
FAU - Ishikawa, Sho
AU  - Ishikawa S
FAU - Hashimoto, Shin-ichi
AU  - Hashimoto S
FAU - Gao, Ji-Liang
AU  - Gao JL
FAU - Murphy, Philip
AU  - Murphy P
FAU - Matsushima, Kouji
AU  - Matsushima K
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Natl Cancer Inst
JT  - Journal of the National Cancer Institute
JID - 7503089
RN  - 0 (CCR1 protein, human)
RN  - 0 (Ccr1 protein, mouse)
RN  - 0 (Chemokine CCL3)
RN  - 0 (Chemokine CCL4)
RN  - 0 (Macrophage Inflammatory Proteins)
RN  - 0 (Receptors, CCR1)
RN  - 0 (Receptors, CCR5)
RN  - 0 (Receptors, Chemokine)
RN  - 0 (Recombinant Proteins)
RN  - 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
SB  - IM
MH  - Animals
MH  - Cell Line, Tumor
MH  - Chemokine CCL3
MH  - Chemokine CCL4
MH  - Dendritic Cells/*metabolism
MH  - Female
MH  - Granulocyte-Macrophage Colony-Stimulating Factor/pharmacology
MH  - Humans
MH  - Immunophenotyping
MH  - Immunotherapy/*methods
MH  - Macrophage Inflammatory Proteins/administration & dosage/metabolism/*pharmacology
MH  - Melanoma, Experimental/*drug therapy/*immunology/metabolism
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred Strains
MH  - Monocytes/metabolism
MH  - Receptors, CCR1
MH  - Receptors, CCR5/*genetics
MH  - Receptors, Chemokine/*genetics
MH  - Recombinant Proteins/administration & dosage/metabolism/pharmacology
MH  - T-Lymphocytes, Cytotoxic
EDAT- 2004/02/05 05:00
MHDA- 2004/02/28 05:00
CRDT- 2004/02/05 05:00
PHST- 2004/02/05 05:00 [pubmed]
PHST- 2004/02/28 05:00 [medline]
PHST- 2004/02/05 05:00 [entrez]
AID - 10.1093/jnci/djh024 [doi]
PST - ppublish
SO  - J Natl Cancer Inst. 2004 Feb 4;96(3):201-9. doi: 10.1093/jnci/djh024.