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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.
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Submitted January 20, 2004
Accepted April 13, 2004
Pleiotropic consequences of Bruton's tyrosine kinase deficiency in myeloid lineages lead to poor inflammatory responses
Anita Mangla, Anupriya Khare, Varanasi Vineeth, Nagesh N Panday, Asok Mukhopadhyay, Balachandran Ravindran, Vineeta Bal*, Anna George, and Satyajit Rath
National Institute of Immunology, New Delhi, India
Regional Medical Research Centre, Bhubaneswar, India
* Corresponding author; email: vineeta{at}nii.res.in.
Bruton's 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 (ROI). 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 sulphate sodium (DSS)-induced colitis, and carrageenan-induced acute edema. Also, polymorphonuclear neutrophil granulocytes (PMNs) in XID mice show poor ROI and NO induction, along with 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 non-infectious inflammatory events in vivo.
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