Abnormal Chemokine-induced Responses of Immature and Mature Hematopoietic Cells from Motheaten Mice Implicate the Protein Tyrosine Phosphatase SHP-1 in Chemokine Responses

doi:10.1084/jem.190.5.681

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© The Rockefeller University Press, 0022-1007/1999/9/681/ $5.00
The Journal of Experimental Medicine, Volume 190, Number 5, September 6, 1999 681-690

Abnormal Chemokine-induced Responses of Immature and Mature Hematopoietic Cells from Motheaten Mice Implicate the Protein Tyrosine Phosphatase SHP-1 in Chemokine Responses

Chang H. Kim^a,b,d,e, Cheng-Kui Qu^c,d,e, Giao Hangoc^a,b,d,e, Scott Cooper^a,b,d,e, Naoyuki Anzai^a,b,d,e, Gen-Sheng Feng^c,d,e, and Hal E. Broxmeyer^a,b,d,e
^a From the Department of Microbiology/Immunology, Indiana University School of Medicine, Indianapolis, Indiana 46202
^b From the Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana 46202
^c From the Department of Biochemistry/Molecular Biology, Indiana University School of Medicine, Indianapolis, Indiana 46202
^d From the Walther Oncology Center, Indiana University School of Medicine, Indianapolis, Indiana 46202
^e Walther Cancer Institute, Indianapolis, Indiana 46208

Correspondence to: Hal E. Broxmeyer, Department of Microbiology/Immunology and the Walther Oncology Center, Indiana University School of Medicine, Bldg. R4, Rm. 302, 1044 West Walnut St., Indianapolis, IN 46202. Tel:317-274-7510 Fax:317-274-7592 E-mail:hbroxmey{at}iupui.edu.

Chemokines regulate a number of biological processes, includingtrafficking of diverse leukocytes and proliferation of myeloidprogenitor cells. SHP-1 (Src homology 2 domain tyrosine phosphatase1), a phosphotyrosine phosphatase, is considered an importantregulator of signaling for a number of cytokine receptors. Sincespecific tyrosine phosphorylation of proteins is important forbiological activities induced by chemokines, we examined therole of SHP-1 in functions of chemokines using viable motheaten(me^v/me^v) mice that were deficient in SHP-1. Chemotactic responsesto stromal call–derived factor 1 (SDF-1), a CXC chemokine,were enhanced with bone marrow myeloid progenitor cells as wellas macrophages, T cells, and B cells from me^v/me^v versus wild-type(+/+) mice. SDF-1–dependent actin polymerization and activationof mitogen-activated protein kinases were also greater in me^v/me^vversus +/+ cells. In contrast, immature subsets of me^v/me^v bonemarrow myeloid progenitors were resistant to effects of a numberof chemokines that suppressed proliferation of +/+ progenitors.These altered chemokine responses did not appear to be due toenhanced expression of CXCR4 or lack of chemokine receptor expression.However, expression of some chemokine receptors (CCR1, CCR2,CCR3, and CXCR2) was significantly enhanced in me^v/me^v T cells.Our results implicate SHP-1 involvement in a number of differentchemokine-induced biological activities.

Key Words: chemokine, Src homology 2 domain tyrosine phosphatase 1, viablemotheaten mice, chemotaxis, myelosuppression, stromal cell–derivedfactor 1

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