| First Author | Tan AH | Year | 2014 |
| Journal | Cell Rep | Volume | 9 |
| Issue | 1 | Pages | 24-31 |
| PubMed ID | 25263549 | Mgi Jnum | J:218547 |
| Mgi Id | MGI:5617901 | Doi | 10.1016/j.celrep.2014.08.043 |
| Citation | Tan AH, et al. (2014) Aberrant presentation of self-lipids by autoimmune B cells depletes peripheral iNKT cells. Cell Rep 9(1):24-31 |
| abstractText | Invariant natural killer T (iNKT) cells provide cognate help via CD1d to lipid antigen-presenting B cells for antibody production, but whether B cells reciprocally regulate iNKT cells remains largely unexplored. Here, we found peripheral, but not thymic, iNKT cells to be numerically reduced in autoimmune mice lacking Fas specifically in B cells. The residual iNKT cells were antigenically overstimulated, had altered cytokine production, and manifested enhanced proliferation and apoptosis. B cell-specific ablation of CD1d ameliorated these iNKT defects, suggesting that inappropriate presentation of CD1d-restricted self-lipids by autoimmune B cell-depleted peripheral iNKT cells. CD1d(+) autoimmune B cells have reduced alpha-galactosidase A expression and, as revealed by lipidomic profiling, altered lipidome with aberrant accumulation of certain self-lipids and reduction of others. These findings unveil a critical link between autoimmunity, B cell lipidome, and the maintenance of peripheral iNKT cells and highlight an essential homeostatic function of B cells beyond antibody production. |
