PMID- 20050333
OWN - NLM
STAT- MEDLINE
DCOM- 20100225
LR  - 20211020
IS  - 1365-2567 (Electronic)
IS  - 0019-2805 (Print)
IS  - 0019-2805 (Linking)
VI  - 129
IP  - 1
DP  - 2010 Jan
TI  - The function of CCR3 on mouse bone marrow-derived mast cells in vitro.
PG  - 115-24
LID - 10.1111/j.1365-2567.2009.03151.x [doi]
AB  - The mechanisms governing the population of tissues by mast cells are not fully 
      understood, but several studies using human mast cells have suggested that 
      expression of the chemokine receptor CCR3 and migration to its ligands may be 
      important. In CCR3-deficient mice, a change in mast cell tissue distribution in 
      the airways following allergen challenge was reported compared with wild-type 
      mice. In addition, there is evidence that CCR3 is important in mast cell 
      maturation in mouse. In this study, bone marrow-derived mast cells (BMMCs) were 
      cultured and CCR3 expression and the migratory response to CCR3 ligands were 
      characterized. In addition, BMMCs were cultured from wild-type and CCR3-deficient 
      mice and their phenotype and migratory responses were compared. CCR3 messenger 
      RNA was detectable in BMMCs, but this was not significantly increased after 
      activation by immunoglobulin E (IgE). CCR3 protein was not detected on BMMCs 
      during maturation and expression could not be enhanced after IgE activation. 
      Resting and IgE-activated immature and mature BMMCs did not migrate in response 
      to the CCR3 ligands eotaxin- 1 and eotaxin-2. Comparing wild-type and 
      CCR3-deficient BMMCs, there were no differences in mast cell phenotype or ability 
      to migrate to the mast cell chemoattractants leukotriene B4 and stem cell factor. 
      The results of this study show that CCR3 may not mediate mast cell migration in 
      mouse BMMCs in vitro. These observations need to be considered in relation to the 
      findings of CCR3 deficiency on mast cells in vivo.
FAU - Collington, Sarah J
AU  - Collington SJ
AD  - Leukocyte Biology Section, MRC & Asthma UK Centre in Allergic Mechanisms of 
      Asthma, National Heart and Lung Institute, Faculty of Medicine, Imperial College 
      London, South Kensington, London, UK. sarah.collington@imperial.ac.uk
FAU - Westwick, John
AU  - Westwick J
FAU - Williams, Timothy J
AU  - Williams TJ
FAU - Weller, Charlotte L
AU  - Weller CL
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Immunology
JT  - Immunology
JID - 0374672
RN  - 0 (Ccr3 protein, mouse)
RN  - 0 (Chemokine CCL11)
RN  - 0 (Chemokine CCL24)
RN  - 0 (Receptors, CCR3)
RN  - 0 (Stem Cell Factor)
RN  - 1HGW4DR56D (Leukotriene B4)
RN  - 37341-29-0 (Immunoglobulin E)
SB  - IM
MH  - Animals
MH  - Bone Marrow/metabolism/pathology
MH  - Cell Migration Assays
MH  - Cells, Cultured
MH  - Chemokine CCL11/metabolism
MH  - Chemokine CCL24/metabolism
MH  - Female
MH  - Immunoglobulin E/immunology
MH  - Leukotriene B4/*metabolism
MH  - Mast Cells/*metabolism/pathology
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Knockout
MH  - Receptors, CCR3/genetics/immunology/*metabolism
MH  - Stem Cell Factor/*metabolism
PMC - PMC2807492
EDAT- 2010/01/06 06:00
MHDA- 2010/02/26 06:00
PMCR- 2011/01/01
CRDT- 2010/01/06 06:00
PHST- 2010/01/06 06:00 [entrez]
PHST- 2010/01/06 06:00 [pubmed]
PHST- 2010/02/26 06:00 [medline]
PHST- 2011/01/01 00:00 [pmc-release]
AID - 10.1111/j.1365-2567.2009.03151.x [doi]
PST - ppublish
SO  - Immunology. 2010 Jan;129(1):115-24. doi: 10.1111/j.1365-2567.2009.03151.x.