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Updated: Jul 12, 2026
Murine Model of CD40-activation of B cells
Published on: March 5, 2010
Ligation of CD200R by CD200 is not required for normal murine myelopoiesis
Eva S K Rijkers1, Talitha de Ruiter, Miranda Buitenhuis
1Department of Immunology, University Medical Centre Utrecht, Utrecht, The Netherlands.
Abstract:
CD200R is an inhibitory receptor involved in the regulation of myeloid cells. It recruits Dok-1 and Dok-2, which are potent inhibitors of the Ras signalling pathway used by colony-stimulating factor (CSF) receptors. Dok-1/Dok-2 double knockout (DKO) mice develop leukaemia at 10-12 months of age. We investigated whether disturbed CD200R signalling could be responsible for this phenotype. Therefore, we studied whether CD200(-/-) mice have altered myelopoiesis and develop leukaemia. We report that CD200R is expressed on haematopoietic progenitor cells. However, CD200(-/-) mice have normal numbers of myeloid progenitors in the bone marrow and these cells have normal proliferative capacity. These results indicate that the development of leukaemia in Dok-1/Dok-2 DKO mice is not solely due to an absence of CD200R signalling. In addition, we show that the previously reported enhanced numbers of myeloid cells do not occur in all CD200(-/-) mice. We determined whether variations in the numbers of peripheral myeloid cells were due to an enhanced response to granulocyte-CSF (G-CSF) or an inflammatory stimulus. Mobilisation of immature neutrophils via G-CSF and infiltration of mature neutrophils and macrophages upon thioglycolate injection were not altered in CD200(-/-) mice. We conclude that CD200(-/-) mice exhibit normal myelopoiesis and that development of leukaemia in Dok-1/Dok-2 DKO mice is not caused by a lack of CD200-mediated CD200R signalling.
Insights
Absence of CD200 receptor (CD200R) signaling does not cause leukemia in mice. Studies show CD200-deficient mice have normal myeloid cell development, ruling out CD200R signaling as the sole cause of leukemia in Dok-1/Dok-2 double knockout mice.
Area of Science:
- Immunology
- Hematology
- Molecular Biology
Background:
- CD200R is an inhibitory receptor regulating myeloid cells by recruiting Dok-1 and Dok-2, inhibitors of Ras signaling.
- Dok-1/Dok-2 double knockout (DKO) mice develop leukemia, suggesting a potential role for CD200R signaling.
- CD200R signaling is crucial for maintaining immune homeostasis and preventing aberrant myeloid cell proliferation.
Purpose of the Study:
- To investigate if disrupted CD200R signaling contributes to leukemia development in Dok-1/Dok-2 DKO mice.
- To determine if CD200-deficient (CD200(-/-)) mice exhibit altered myelopoiesis or develop leukemia.
- To assess the role of CD200R signaling in myeloid progenitor cell function and response to stimuli.
Main Methods:
- Analysis of hematopoietic progenitor cells in CD200(-/-) mice.
- Assessment of myeloid progenitor cell proliferation capacity.
- Evaluation of peripheral myeloid cell numbers and response to granulocyte-colony stimulating factor (G-CSF) and inflammatory stimuli (thioglycolate injection).
Main Results:
- CD200R is expressed on hematopoietic progenitor cells.
- CD200(-/-) mice display normal numbers and proliferative capacity of myeloid progenitors.
- Mobilization of neutrophils and infiltration of myeloid cells in response to G-CSF and thioglycolate were not altered in CD200(-/-) mice.
Conclusions:
- CD200(-/-) mice exhibit normal myelopoiesis.
- The development of leukemia in Dok-1/Dok-2 DKO mice is not solely caused by the absence of CD200-mediated CD200R signaling.
- CD200R signaling is not essential for normal myeloid cell development or response to G-CSF and inflammatory stimuli.
