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Published on: March 6, 2010
CD72-deficient mice reveal nonredundant roles of CD72 in B cell development and activation
C Pan1, N Baumgarth, J R Parnes
1Department of Medicine, Stanford University School of Medicine, California 94305, USA.
Insights
CD72 is crucial for B cell development and activation. CD72-deficient mice show altered B cell populations and hyperresponsive B cells, highlighting CD72
Area of Science:
- Immunology
- Cell Biology
- Biochemistry
Background:
- CD72 is a B cell surface protein belonging to the C-type lectin superfamily.
- It interacts with the tyrosine phosphatase SHP-1 via its ITIM motif.
Purpose of the Study:
- To investigate the role of CD72 in B cell development and activation using CD72-deficient mice.
Main Methods:
- Utilized CD72-deficient (CD72-/-) mice.
- Analyzed B cell populations in bone marrow and periphery.
- Assessed B cell activation in response to stimuli and intracellular Ca2+ flux.
Main Results:
- CD72 deficiency led to reduced mature recirculating B cells and accumulated pre-B cells in bone marrow.
- Peripheral B cell populations showed fewer mature B-2 cells and more B-1 cells in CD72-/- mice.
- CD72-/- B cells exhibited hyperproliferation and enhanced Ca2+ responses upon activation.
Conclusions:
- CD72 is a nonredundant regulator of B cell development.
- CD72 negatively regulates B cell activation, controlling proliferation and signaling responses.
Abstract:
CD72, a B cell surface protein of the C-type lectin superfamily, recruits the tyrosine phosphatase SHP-1 through its ITIM motif(s). Using CD72-deficient (CD72-/-) mice, we demonstrate that CD72 is a nonredundant regulator of B cell development. In the bone marrow of CD72-/- mice, there was a reduction in the number of mature recirculating B cells and an accumulation of pre-B cells. In the periphery of CD72-/- mice, there were fewer mature B-2 cells and more B-1 cells. In addition, CD72 is a negative regulator of B cell activation, as CD72-/- B cells were hyperproliferative in response to various stimuli and showed enhanced kinetics in their intracellular Ca2+ response following IgM cross-linking.
