PMID- 23646151
OWN - NLM
STAT- MEDLINE
DCOM- 20131126
LR  - 20211021
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 8
IP  - 4
DP  - 2013
TI  - Uncoupling of natural IgE production and CD23 surface expression levels.
PG  - e62851
LID - 10.1371/journal.pone.0062851 [doi]
LID - e62851
AB  - CD23, the low affinity receptor for immunoglobulin E (IgE), has been proposed to 
      play a critical role in the regulation of IgE production, based on altered IgE 
      levels in CD23-deficient mice and transgenic mouse models, as well as in mouse 
      strains with mutations in the CD23 gene, e.g. 129 substrains. Here, we have 
      investigated a mouse line termed LxT1 that expresses reduced CD23 surface levels 
      on B cells, and its influence on natural IgE production. Extensive phenotypic 
      analysis showed that CD23 surface expression was reduced in LxT1 compared to the 
      control, without affecting B cell development in general. This CD23(low) surface 
      level in LxT1 mice is not as a result of reduced CD23 mRNA expression levels or 
      intracellular accumulation, but linked to a recessive locus, a 129-derived region 
      spanning 28 Mb on chromosome 8, which includes the CD23 gene. Sequence analysis 
      confirmed five mutations within the CD23 coding region in LxT1 mice, the same as 
      those present in New Zealand Black (NZB) and 129 mice. However, this CD23(low) 
      phenotype was not observed in all 129 substrains despite carrying these same CD23 
      mutations in the coding region. Moreover, serum IgE levels in LxT1 mice are as 
      low as those in the C57BL/6 (B6) strain, and much lower than those in 129 
      substrains. These data indicate that the CD23 surface level and serum IgE level 
      are uncoupled and that neither is directly regulated by the mutations within the 
      CD23 coding region. This study suggests that caution should be taken when 
      interpreting the immunological data derived from mice with different genetic 
      background, especially if the gene of interest is thought to influence CD23 
      surface expression or serum IgE level.
FAU - Ren, Weicheng
AU  - Ren W
AD  - Department of Rheumatology and Inflammation Research, University of Gothenburg, 
      Gothenburg, Sweden.
FAU - Lagerstedt, Kristina
AU  - Lagerstedt K
FAU - Grimsholm, Ola
AU  - Grimsholm O
FAU - Stern, Anna
AU  - Stern A
FAU - Sun, Jia-Bin
AU  - Sun JB
FAU - Fang, Yu
AU  - Fang Y
FAU - Xiang, Zou
AU  - Xiang Z
FAU - Martensson, Inga-Lill
AU  - Martensson IL
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130430
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Membrane Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, IgE)
RN  - 37341-29-0 (Immunoglobulin E)
RN  - EC 3.4.- (Amyloid Precursor Protein Secretases)
RN  - EC 3.4.24.- (ADAM Proteins)
RN  - EC 3.4.24.81 (ADAM10 Protein)
RN  - EC 3.4.24.81 (Adam10 protein, mouse)
SB  - IM
MH  - ADAM Proteins/genetics/metabolism
MH  - ADAM10 Protein
MH  - Amyloid Precursor Protein Secretases/genetics/metabolism
MH  - Animals
MH  - B-Lymphocytes/immunology/metabolism
MH  - Chromosomes, Mammalian
MH  - Female
MH  - Immunoglobulin E/*biosynthesis/blood
MH  - Intracellular Space/metabolism
MH  - Male
MH  - Membrane Proteins/genetics/metabolism
MH  - Mice
MH  - Mice, 129 Strain
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Mice, Transgenic
MH  - Mutation
MH  - Open Reading Frames
MH  - Phenotype
MH  - RNA, Messenger/genetics/metabolism
MH  - Receptors, IgE/genetics/*metabolism
MH  - Spleen/cytology/immunology
PMC - PMC3639908
COIS- Competing Interests: AFA Insurance is an organisation owned by Sweden's labour 
      market parties. They insure employees within the private sector, municipalities 
      and county councils. AFA supports research in the areas of work environment and 
      health. None of the authors are employed by or act as consultant for AFA. The 
      authors do not have any AFA related patents, products in development or marketed 
      products. The authors confirm that this does not alter their adherence to all the 
      PLOS ONE policies on sharing data and materials.
EDAT- 2013/05/07 06:00
MHDA- 2013/12/16 06:00
PMCR- 2013/04/30
CRDT- 2013/05/07 06:00
PHST- 2012/12/12 00:00 [received]
PHST- 2013/03/26 00:00 [accepted]
PHST- 2013/05/07 06:00 [entrez]
PHST- 2013/05/07 06:00 [pubmed]
PHST- 2013/12/16 06:00 [medline]
PHST- 2013/04/30 00:00 [pmc-release]
AID - PONE-D-12-39814 [pii]
AID - 10.1371/journal.pone.0062851 [doi]
PST - epublish
SO  - PLoS One. 2013 Apr 30;8(4):e62851. doi: 10.1371/journal.pone.0062851. Print 2013.