It is widely admitted that the non steroidal anti-inflammatory drugs (NSAID) inhibits the synthesis of prostaglandins by blocking the membrane cyclo-oxygenase. The anti-inflammatory activity of these molecules is partly explained by the vaso-dilatational action of PG2 in particular. However this effect alone cannot account for all the properties of NSAID. The latter have an inhibitory action at the level of the various functions of neurophil leucocytes and to a lesser degree at the level of macrophages. For immune system itself, it seems the NSAID have a rather immunostimulant effect due to a major action on T lymphocytes. In the course of rheumatoid arthritis (RA), the NSAID are unable to modify the ratio CD4/CD8. Yet they may decrease the production of the rheumatoid factor (RF). This ability is related to a loss of the normal suppressive T cells inhibition exerted by PG. Besides the NSAID seem unable to modify the natural killer function (NK). Finally, the impact on the synthesis of interleukins (IL) notably 1 and 2 does not seem clear. Indeed several research papers give us contradictory results between animals and men and between physiological or pathological situations.