Macrophages are highly plastic cells who can change their fenotype and metabolism due to environmental stimuli present in the tissue they enhabit. Cellular programs they have established are not final and macrophages can adapt to new conditions with the aim of maintaining homeostasis. There is a spectrum of macrophage populations but, due to their activation modes and gene expression profiles, they can be diveded in two simplified groups; inflammatory M1 phenotype and anti-inflammatory M2 phenotype. Ratio immbalances of M1 and M2 populations have been observed in some autoimmune diseases such as rheumatoid arthritis, systemic lupus erythematosus and ulcerative colitis. With decreased number of M2 macrophages and prolonged activation of M1 macrophages establishment of homeostasis is delayed and time between relapses is reduced. Nowadays, the most prominent methods for treating autoimmune diseases are based on immunosuppressants. Alternative aproach could be reestablishment of favorable M1/M2 ratio. Experiments showed promising results when researchers induced M1 cellular death or reprogrammed them into M2 but further development of higher specificity in targeting certain populations is necessary