| First Author | Liu Z | Year | 2019 |
| Journal | Int Immunol | Volume | 31 |
| Issue | 11 | Pages | 715-728 |
| PubMed ID | 31081901 | Mgi Jnum | J:280382 |
| Mgi Id | MGI:6364675 | Doi | 10.1093/intimm/dxz041 |
| Citation | Liu Z, et al. (2019) Cmtm7 knockout inhibits B-1a cell development at the transitional (TrB-1a) stage. Int Immunol 31(11):715-728 |
| abstractText | Innate-like B-1a cells are an important cell population for production of natural IgM and interleukin-10 (IL-10), and act as the first line against pathogens. We determined that CMTM7 is essential for B-1a cell development. Following Cmtm7 (CKLF-like MARVEL transmembrane domain-containing 7) knockout, B-1a cell numbers decreased markedly in all investigated tissues. Using a bone marrow and fetal liver adoptive transfer model and conditional knockout mice, we showed that the reduction of B-1a cells resulted from B-cell-intrinsic defects. Because of B-1a cell loss, Cmtm7-deficient mice produced less IgM and IL-10, and were more susceptible to microbial sepsis. Self-renewal and homeostasis of mature B-1a cells in Cmtm7-/- mice were not impaired, suggesting the effect of Cmtm7 on B-1a cell development. Further investigations demonstrated that the function of Cmtm7 in B-1a cell development occurred at the specific transitional B-1a (TrB-1a) stage. Cmtm7 deficiency resulted in a slow proliferation and high cell death rate of TrB-1a cells. Thus, Cmtm7 controls B-1a cell development at the transitional stage. |
