Abstract
Cladribine represents a novel possibility of multiple sclerosis treatment. Mechanism of action is derived from observation of adenosindeaminase deficiency in severe combined immunodeficit.
Cladribin exerts incomplete depletion of both activated and restingT- and B- lymphocytes, with repopulation which induces long-term shift in immune system function including change in cytokineproduction. When this effect is compared with alemtuzumab we observe difference in repopulation of B lymphocytes which donot jump above baseline values in patients treated with cladribine.
This may explain no occurence of secondary autoimmunities.