{'fraction_non_alphanumeric': 0.025423728813559324, 'fraction_numerical': 0.002421307506053269, 'mean_word_length': 5.2180451127819545, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Future directions in the study of fingolimod in multiple sclerosis

The efficacy of fingolimod treatment for multiple sclerosis (MS) has been shown, but its exact mechanism remains unclear. Fingolimod is an oral disease‐modifying drug that prevents the entry of autoreactive T cells into the central nervous system (CNS) by inhibiting the egress of T cells from the lymph nodes. It binds sphingosine‐1‐phosphate (S1P) receptors on a variety of cells, including cells in the CNS, where it exerts diverse effects. In addition to its immune mechanisms, recent studies suggested that non‐immune mechanisms might play a role in the efficacy of fingolimod for the treatment of MS. Herein, we explore the underlying mechanisms of fingolimod in MS, which will therefore improve the understanding of its beneficial and adverse effects.