CD72-deficient mice reveal nonredundant roles of CD72 in B cell development and activation

Immunity. 1999 Oct;11(4):495-506. doi: 10.1016/s1074-7613(00)80124-7.


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.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Antibody Formation
  • Antigens, CD / genetics
  • Antigens, CD / physiology*
  • Antigens, Differentiation, B-Lymphocyte / genetics
  • Antigens, Differentiation, B-Lymphocyte / physiology*
  • B-Lymphocyte Subsets / cytology*
  • B-Lymphocyte Subsets / immunology
  • Blood Cells
  • Bone Marrow / pathology
  • Calcium Signaling
  • Cell Differentiation
  • Female
  • Immunoglobulin M / immunology
  • Immunologic Capping
  • Lymphocyte Activation*
  • Lymphoid Tissue / pathology
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Inbred CBA
  • Mice, Knockout


  • Antigens, CD
  • Antigens, Differentiation, B-Lymphocyte
  • CD72 protein, human
  • Immunoglobulin M