Rebound of disease activity after fingolimod withdrawal: Immunological and gene expression profiling.Sacco R, Emming S, Gobbi C, Zecca C, Monticelli S.Mult Scler Relat Disord. 2020 Jan 3;40:101927
Discontinuation of disease-modifying therapy with fingolimod can lead to severe Multiple Sclerosis (MS) rebound activity; however, this phenomenon remains mechanistically incompletely understood (fingolimod traps B cells in lymph glands and bone marrow and you stop fingolimod and the cells enter the blood and get into the brain and a relapse occurs…rituximab gets rid of the B cells. So there’s a start), and the short-term impact of a therapy switch on inflammatory gene expression in T lymphocytes is unknown (You could say who cares you are not looking at the right cell type, so another good example how T cell blinkers abound). We present the clinico-radiological and immunological description of a case of rebound activity after fingolimod discontinuation and switching to rituximab treatment in a relapsing-remitting MS patient (Why would a B cell depleting strategy be so successful if the issue were T cells…I guess you will say it is the 1% of CD4 T cells affected that are the key). After severe rebound (A plan should be inplace when fingolomod or natalizumab is stopped and people should switch , a reduction in the expression of inflammatory cbefore rebound occurs) cytokines and transcription factors was rapidly observed after administration of methylprednisolone and rituximab. Rituximab led to an effective suppression of inflammatory activity, and at least in this specific case it represented a valid switching approach after fingolimod discontinuation (There are anumber of other studies saying the same thing).