PubTransformer

A site to transform Pubmed publications into these bibliographic reference formats: ADS, BibTeX, EndNote, ISI used by the Web of Knowledge, RIS, MEDLINE, Microsoft's Word 2007 XML.

The lack of BTK does not impair monocytes and polymorphonuclear cells functions in X-linked agammaglobulinemia under treatment with intravenous immunoglobulin replacement.

Abstract The lack of BTK in X-linked agammaglobulinemia (XLA) patients does not affect monocytes and polymorphonuclear cells (PMN) phenotype and functions. In this study, we show that XLA patients had an increased frequency of the intermediate monocytes subset and that BTK-deficient monocytes and PMN had a normal expression of receptors involved in the activation and cellular responses. We demonstrate that BTK is not required for migration, phagocytosis and the production of reactive oxygen species (ROS) following engagement of FC gamma receptors (FcγR). XLA monocytes and PMN showed an efficient calcium (Ca2+)-independent activation of oxidative burst, suggesting that oxidative burst is less dependent by Ca2+ mobilization. The phagocytosis was functional and it remained unaltered also after Ca2+ chelation, confirming the independence of phagocytosis on Ca2+ mobilization. Intravenous immunoglobulin (IVIg) infusion exerted an anti-inflammatory effect by reducing the frequency of pro-inflammatory monocytes. In monocytes, the IVIg reduce the oxidative burst and phagocytosis even if these functions remained efficient.
PMID
Related Publications
Authors

Mayor MeshTerms
Keywords
Journal Title plos one
Publication Year Start




PMID- 28422989
OWN - NLM
STAT- In-Process
DA  - 20170419
LR  - 20170419
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 12
IP  - 4
DP  - 2017
TI  - The lack of BTK does not impair monocytes and polymorphonuclear cells functions
      in X-linked agammaglobulinemia under treatment with intravenous immunoglobulin
      replacement.
PG  - e0175961
LID - 10.1371/journal.pone.0175961 [doi]
AB  - The lack of BTK in X-linked agammaglobulinemia (XLA) patients does not affect
      monocytes and polymorphonuclear cells (PMN) phenotype and functions. In this
      study, we show that XLA patients had an increased frequency of the intermediate
      monocytes subset and that BTK-deficient monocytes and PMN had a normal expression
      of receptors involved in the activation and cellular responses. We demonstrate
      that BTK is not required for migration, phagocytosis and the production of
      reactive oxygen species (ROS) following engagement of FC gamma receptors
      (FcgammaR). XLA monocytes and PMN showed an efficient calcium (Ca2+)-independent 
      activation of oxidative burst, suggesting that oxidative burst is less dependent 
      by Ca2+ mobilization. The phagocytosis was functional and it remained unaltered
      also after Ca2+ chelation, confirming the independence of phagocytosis on Ca2+
      mobilization. Intravenous immunoglobulin (IVIg) infusion exerted an
      anti-inflammatory effect by reducing the frequency of pro-inflammatory monocytes.
      In monocytes, the IVIg reduce the oxidative burst and phagocytosis even if these 
      functions remained efficient.
FAU - Cavaliere, Filomena Monica
AU  - Cavaliere FM
AD  - Department of Molecular Medicine, Sapienza University of Rome, Roma, Italy.
FAU - Prezzo, Alessandro
AU  - Prezzo A
AD  - Department of Molecular Medicine, Sapienza University of Rome, Roma, Italy.
FAU - Bilotta, Caterina
AU  - Bilotta C
AD  - Department of Molecular Medicine, Sapienza University of Rome, Roma, Italy.
FAU - Iacobini, Metello
AU  - Iacobini M
AD  - Department of Pediatrics, Sapienza University of Rome, Roma, Italy.
FAU - Quinti, Isabella
AU  - Quinti I
AD  - Department of Molecular Medicine, Sapienza University of Rome, Roma, Italy.
LA  - eng
PT  - Journal Article
DEP - 20170419
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
EDAT- 2017/04/20 06:00
MHDA- 2017/04/20 06:00
CRDT- 2017/04/20 06:00
PHST- 2016/09/29 [received]
PHST- 2017/04/03 [accepted]
AID - 10.1371/journal.pone.0175961 [doi]
AID - PONE-D-16-38472 [pii]
PST - epublish
SO  - PLoS One. 2017 Apr 19;12(4):e0175961. doi: 10.1371/journal.pone.0175961.
      eCollection 2017.

<?xml version="1.0" encoding="UTF-8"?>
<b:Sources SelectedStyle="" xmlns:b="http://schemas.openxmlformats.org/officeDocument/2006/bibliography"  xmlns="http://schemas.openxmlformats.org/officeDocument/2006/bibliography" >
</b:Sources>