Source:http://linkedlifedata.com/resource/pubmed/id/21063022
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
|
pubmed:dateCreated |
2011-1-28
|
pubmed:abstractText |
Bruton tyrosine kinase (Btk) is essential for B cell development and function and also appears to be important for myeloid cells. The bone marrow of Btk-deficient mice shows enhanced granulopoiesis compared with that of wild-type mice. In purified granulocyte-monocyte-progenitors (GMP) from Btk-deficient mice, the development of granulocytes is favored at the expense of monocytes. However, Btk-deficient neutrophils are impaired in maturation and function. Using bone marrow chimeras, we show that this defect is cell-intrinsic to neutrophils. In GMP and neutrophils, Btk plays a role in GM-CSF- and Toll-like receptor-induced differentiation. Molecular analyses revealed that expression of the lineage-determining transcription factors C/EBP?, C/EBP?, and PU.1, depends on Btk. In addition, expression of several granule proteins, including myeloperoxidase, neutrophilic granule protein, gelatinase and neutrophil elastase, is Btk-dependent. In the Arthus reaction, an acute inflammatory response, neutrophil migration into tissues, edema formation, and hemorrhage are significantly reduced in Btk-deficient animals. Together, our findings implicate Btk as an important regulator of neutrophilic granulocyte maturation and function in vivo.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
AIM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Agammaglobulinaemia tyrosine kinase,
http://linkedlifedata.com/resource/pubmed/chemical/Granulocyte-Macrophage...,
http://linkedlifedata.com/resource/pubmed/chemical/Protein-Tyrosine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptors
|
pubmed:status |
MEDLINE
|
pubmed:month |
Jan
|
pubmed:issn |
1528-0020
|
pubmed:author | |
pubmed:issnType |
Electronic
|
pubmed:day |
27
|
pubmed:volume |
117
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
1329-39
|
pubmed:dateRevised |
2011-11-2
|
pubmed:meshHeading |
pubmed-meshheading:21063022-Agammaglobulinemia,
pubmed-meshheading:21063022-Animals,
pubmed-meshheading:21063022-Bone Marrow Cells,
pubmed-meshheading:21063022-Cell Differentiation,
pubmed-meshheading:21063022-Cells, Cultured,
pubmed-meshheading:21063022-Disease Models, Animal,
pubmed-meshheading:21063022-Genetic Diseases, X-Linked,
pubmed-meshheading:21063022-Granulocyte-Macrophage Colony-Stimulating Factor,
pubmed-meshheading:21063022-Mice,
pubmed-meshheading:21063022-Mice, Inbred C57BL,
pubmed-meshheading:21063022-Mice, Inbred CBA,
pubmed-meshheading:21063022-Mice, Transgenic,
pubmed-meshheading:21063022-Neutrophils,
pubmed-meshheading:21063022-Protein-Tyrosine Kinases,
pubmed-meshheading:21063022-Toll-Like Receptors
|
pubmed:year |
2011
|
pubmed:articleTitle |
Neutrophil development and function critically depend on Bruton tyrosine kinase in a mouse model of X-linked agammaglobulinemia.
|
pubmed:affiliation |
Institute of Physiological Chemistry, Ulm University, Albert-Einstein-Allee 11, Ulm, Germany.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|