| First Author | Tesfagiorgis Y | Year | 2024 |
| Journal | J Neuroimmunol | Volume | 387 |
| Pages | 578267 | PubMed ID | 38155065 |
| Mgi Jnum | J:355515 | Mgi Id | MGI:7715062 |
| Doi | 10.1016/j.jneuroim.2023.578267 | Citation | Tesfagiorgis Y, et al. (2024) Systemic administration of anti-CD20 indirectly reduces B cells in the inflamed meninges in a chronic model of central nervous system autoimmunity. J Neuroimmunol 387:578267 |
| abstractText | Anti-CD20 B cell depleting therapies have demonstrated that B cells are important drivers of disease progress in Multiple Sclerosis, although the pathogenic mechanisms are not well understood. A population of B cells accumulates in the inflamed meninges in MS and also some chronic animal models of disease, typically adjacent to demyelinating lesions. The role of these meningeal B cells in disease is not known, nor is their susceptibility to anti-CD20 therapy. Here, we administered anti-CD20 to 2D2 IgH(MOG) spontaneous experimental autoimmune encephalomyelitis mice in the chronic phase of disease, after the establishment of meningeal B cell clusters. Compared to the circulation, lymph nodes, and spleen, B cell depletion from the meninges was delayed and not evident until 7d post-administration of anti-CD20. Further, we did not find evidence that anti-CD20 accessed meningeal B cells directly, but rather that depletion was indirect and the result of ongoing turnover of the meningeal population and elimination of the peripheral pool from which it is sustained. |
