White blood cells circulate round the blood and can enter lymph glands via specilalised blood vessels called high endothelial venules (small vein) blood vessels using a molecule called CD62L which binds to a sugar molecule on the high endothelial cells.
In cases of MS the thought is that these white blood cells then enter the brain and thinking that oligodendrocytes and myelin are infections they cause damage that leads to demyelination and symptoms of MS. Now Gilenya works by blocking the action of a molecule (Sphinosine-1-phosphate receptor) that is a gatekeeper of the efferent lymphatics that stops the white blood cells exiting the lymph gland.
However only the naive and central memory populations, which are thought to be involved in MS, use this molecule to exit the lymph cells, whereas effector memory cells that fight infection do not. Therefore whilst Gilenya is a potent immunosuppressive and can inhibit relapsing disease the hope is that it does not stop one from fighting off infections.
Another way to think of this is to imagine a racing track (blood system) and the pitstop (lymph gland) and the racing cars (white blood cell). Cars have to go into the pitstop to change their tyres and then off they go back to the blood. The team managers can call in the cars by perhaps putting out a flag so the cars come in. The naive (yellow) and central memory (green) cars run on Goodyear tyres whereas the red car (effector memeory) cars run on Pirelli tyres. Now gilenya blocks the Goodyear truck from delivering tryes and so when the cars come into the pits for a tyre change there are no spare tyres and so the yellow and red cars get stuck in the pitstop and have to retire from the race. However, the red car can just keep going and protect against infection.
For those of you interested, below is a video infomercial for Doctors made by Novaritis, which indicates how fingolimod may works. The first half talks about what we have said above.