B cell-specific deletion of protein-tyrosine phosphatase Shp1 promotes B-1a cell development and causes systemic autoimmunity.

@article{Pao2007BCD,
  title={B cell-specific deletion of protein-tyrosine phosphatase Shp1 promotes B-1a cell development and causes systemic autoimmunity.},
  author={Lily I. Pao and Kong-Peng Lam and Joel M Henderson and Jeffery L. Kutok and Marat B. Alimzhanov and Lars Nitschke and Matthew L. Thomas and Benjamin G Neel and K. Rajewsky},
  journal={Immunity},
  year={2007},
  volume={27 1},
  pages={35-48}
}
Spontaneous loss-of-function mutations in the protein-tyrosine phosphatase Shp1 cause the motheaten phenotype, characterized by widespread inflammation and autoimmunity. Because Shp1 is expressed in all hematopoietic cells, it has been unclear which aspects of the motheaten phenotypes are primary effects of Shp1 deficiency. We generated mice (Ptpn6(f/f);CD19-cre) that delete Shp1 specifically in B cells. Analysis of these mice indicates that the increase in B-1a cells in motheaten mice is a… CONTINUE READING