PMID- 10974036
OWN - NLM
STAT- MEDLINE
DCOM- 20000928
LR  - 20220409
IS  - 0022-1007 (Print)
IS  - 1540-9538 (Electronic)
IS  - 0022-1007 (Linking)
VI  - 192
IP  - 5
DP  - 2000 Sep 4
TI  - Macrophage inflammatory protein 3alpha is expressed at inflamed epithelial 
      surfaces and is the most potent chemokine known in attracting Langerhans cell 
      precursors.
PG  - 705-18
AB  - Dendritic cells (DCs) form a network comprising different populations that 
      initiate and differentially regulate immune responses. Langerhans cells (LCs) 
      represent a unique population of DCs colonizing epithelium, and we present here 
      observations suggesting that macrophage inflammatory protein (MIP)-3alpha plays a 
      central role in LC precursor recruitment into the epithelium during inflammation. 
      (a) Among DC populations, MIP-3alpha was the most potent chemokine inducing the 
      selective migration of in vitro-generated CD34(+) hematopoietic progenitor 
      cell-derived LC precursors and skin LCs in accordance with the restricted 
      MIP-3alpha receptor (CC chemokine receptor 6) expression to these cells. (b) 
      MIP-3alpha was mainly produced by epithelial cells, and the migration of LC 
      precursors induced by the supernatant of activated skin keratinocytes was 
      completely blocked with an antibody against MIP-3alpha. (c) In vivo, MIP-3alpha 
      was selectively produced at sites of inflammation as illustrated in tonsils and 
      lesional psoriatic skin where MIP-3alpha upregulation appeared associated with an 
      increase in LC turnover. (d) Finally, the secretion of MIP-3alpha was strongly 
      upregulated by cells of epithelial origin after inflammatory stimuli (interleukin 
      1beta plus tumor necrosis factor alpha) or T cell signals. Results of this study 
      suggest a major role of MIP-3alpha in epithelial colonization by LCs under 
      inflammatory conditions and immune disorders, and might open new ways to control 
      epithelial immunity.
FAU - Dieu-Nosjean, M C
AU  - Dieu-Nosjean MC
AD  - Laboratory for Immunological Research, Schering-Plough, 69571 Dardilly, France.
FAU - Massacrier, C
AU  - Massacrier C
FAU - Homey, B
AU  - Homey B
FAU - Vanbervliet, B
AU  - Vanbervliet B
FAU - Pin, J J
AU  - Pin JJ
FAU - Vicari, A
AU  - Vicari A
FAU - Lebecque, S
AU  - Lebecque S
FAU - Dezutter-Dambuyant, C
AU  - Dezutter-Dambuyant C
FAU - Schmitt, D
AU  - Schmitt D
FAU - Zlotnik, A
AU  - Zlotnik A
FAU - Caux, C
AU  - Caux C
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Exp Med
JT  - The Journal of experimental medicine
JID - 2985109R
RN  - 0 (CCL20 protein, human)
RN  - 0 (CCR6 protein, human)
RN  - 0 (Chemokine CCL20)
RN  - 0 (Chemokines, CC)
RN  - 0 (Macrophage Inflammatory Proteins)
RN  - 0 (Receptors, CCR6)
RN  - 0 (Receptors, Chemokine)
SB  - IM
MH  - Animals
MH  - Cell Line
MH  - Chemokine CCL20
MH  - *Chemokines, CC
MH  - Epithelium/chemistry
MH  - Humans
MH  - Inflammation/*metabolism
MH  - Langerhans Cells/*physiology
MH  - Macrophage Inflammatory Proteins/analysis/*physiology
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Psoriasis/metabolism
MH  - Receptors, CCR6
MH  - Receptors, Chemokine/analysis
MH  - Stem Cells/*physiology
MH  - T-Lymphocytes/physiology
PMC - PMC2193271
EDAT- 2000/09/07 11:00
MHDA- 2000/09/30 11:01
PMCR- 2001/03/05
CRDT- 2000/09/07 11:00
PHST- 2000/09/07 11:00 [pubmed]
PHST- 2000/09/30 11:01 [medline]
PHST- 2000/09/07 11:00 [entrez]
PHST- 2001/03/05 00:00 [pmc-release]
AID - 000411 [pii]
AID - 10.1084/jem.192.5.705 [doi]
PST - ppublish
SO  - J Exp Med. 2000 Sep 4;192(5):705-18. doi: 10.1084/jem.192.5.705.