| First Author | Chen L | Year | 2016 |
| Journal | Immunol Lett | Volume | 172 |
| Pages | 67-78 | PubMed ID | 26921474 |
| Mgi Jnum | J:270419 | Mgi Id | MGI:6200139 |
| Doi | 10.1016/j.imlet.2016.02.015 | Citation | Chen L, et al. (2016) A critical role for the protein kinase PKK in the maintenance of recirculating mature B cells and the development of B1 cells. Immunol Lett 172:67-78 |
| abstractText | Protein kinase C associated kinase (PKK) regulates NF-kappaB activation and is required for the survival of certain lymphoma cells. Mice lacking PKK die soon after birth, and previous studies suggest that the role of PKK in B cell development might be context dependent. We have generated a mouse strain harboring conditional null alleles for PKK and a Cre-recombinase transgene under the control of the endogenous CD19 promoter. In the present study, we show that knockout of PKK in B cells results in the reduction of long-lived recirculating mature B cell population in lymph nodes and bone marrow as well as a decrease in peritoneal B1 cells, while PKK deficiency has no apparent effect on early B cell development in bone marrow or the development of follicular and marginal zone B cells in the spleen. In addition, we demonstrate that PKK-deficient B cells display defective proliferation and survival responses to stimulation of B cell receptor (BCR), which may underlie the reduction of recirculating mature B cells in PKK mutant mice. Consistently, BCR-mediated NF-kappaB activation, known to be required for the survival of activated but not resting B cells, is attenuated in PKK-deficient B cells. Thus, our results reveal a critical role of PKK in the maintenance of recirculating mature B cells as well as the development of B1 cells in mice. |
