|
|
Blood, 15 August 2004, Vol. 104, No. 4, pp. 1191-1197.
Prepublished online as a Blood First Edition Paper on April 29, 2004; DOI 10.1182/blood-2004-01-0207.
 Previous Article | Table of Contents | Next Article 
PHAGOCYTES
Pleiotropic consequences of Bruton tyrosine kinase deficiency in myeloid lineages lead to poor inflammatory responses
Anita Mangla,
Anupriya Khare,
Varanasi Vineeth,
Nagesh Narayan Panday,
Asok Mukhopadhyay,
Balachandran Ravindran,
Vineeta Bal,
Anna George, and
Satyajit Rath
From the National Institute of Immunology, New Delhi, India, and the Regional Medical Research Centre, Bhubaneswar, India.
Bruton tyrosine kinase (Btk), a non-receptor-associated tyrosine kinase of the Tec family, appears to participate in many myeloid cell functions. We show that macrophages from X-linked immunodeficient (XID) mice lacking functional Btk cannot generate efficient bursts of reactive oxygen intermediates (ROIs). The induction of apoptotic cell death by inflammatory stimuli is also enhanced in XID macrophages. Phagocytosis of bacterial particles is only marginally affected in them. In vivo, XID mice show reduced severity of inflammatory diseases in models of experimental autoimmune encephalomyelitis (EAE), dextran sulfate sodium (DSS)-induced colitis, and carrageenan-induced acute edema. Also, polymorphonuclear neutrophil granulocytes (PMNs) in XID mice show poor ROI and nitric oxide (NO) induction, along with a reduction in PMN recruitment to peritoneal inflammation. XID mice show reduction in PMN numbers in peripheral blood, and their bone marrow shows a reduction in the numbers of both monocytic and granulocytic lineages, extending to the earliest progenitor populations. Thus, Btk is likely to play a significant role at multiple points during the development and functioning of the myeloid lineages, affecting the outcome of many infectious as well as noninfectious inflammatory events in vivo. (Blood. 2004;104:1191-1197)
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
M. Melcher, B. Unger, U. Schmidt, I. A. Rajantie, K. Alitalo, and W. Ellmeier
Essential Roles for the Tec Family Kinases Tec and Btk in M-CSF Receptor Signaling Pathways That Regulate Macrophage Survival
J. Immunol.,
June 15, 2008;
180(12):
8048 - 8056.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. Srivastava, H. Banerjee, A. Chaudhry, A. Khare, A. Sarin, A. George, V. Bal, J. M. Durdik, and S. Rath
Apoptosis-Inducing Factor Regulates Death in Peripheral T Cells
J. Immunol.,
July 15, 2007;
179(2):
797 - 803.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
Q. Su, Y. Zhou, and R. A. Johns
Bruton's tyrosine kinase (BTK) is a binding partner for hypoxia induced mitogenic factor (HIMF/FIZZ1) and mediates myeloid cell chemotaxis
FASEB J,
May 1, 2007;
21(7):
1376 - 1382.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
K. Sochorova, R. Horvath, D. Rozkova, J. Litzman, J. Bartunkova, A. Sediva, and R. Spisek
Impaired Toll-like receptor 8-mediated IL-6 and TNF-{alpha} production in antigen-presenting cells from patients with X-linked agammaglobulinemia
Blood,
March 15, 2007;
109(6):
2553 - 2556.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
N. J. Horwood, T. H. Page, J. P. McDaid, C. D. Palmer, J. Campbell, T. Mahon, F. M. Brennan, D. Webster, and B. M. J. Foxwell
Bruton's Tyrosine Kinase Is Required for TLR2 and TLR4-Induced TNF, but Not IL-6, Production
J. Immunol.,
March 15, 2006;
176(6):
3635 - 3641.
[Abstract]
[Full Text]
[PDF]
|
|
|
| |
