Microglial cells (MC) are key immune cells within the central nervous system (CNS).

They participate in CNS homeostasis being able to become activated once they

contact exogenous and endogenous pro-inflammatory signals. After activation, MC

coordinate the inflammatory responses to repair the CNS parenchyma, however,

persistent activation may cause neurodegeneration. Anti-inflammatory cytokines such

as IL-4 and IL-13 may induce ?alternative activation? of MC which regulate neurotoxic

inflammation. Here, we evaluated the effects of IL-4 on the CNS inflammatory

response induced by systemic injections of lipopolysaccharide (LPS) on IL-4 KO mice.

Our preliminary results indicate that MC isolated from IL-4 KO mice showed increased

expression of MHC class II, CD80 and CD86 molecules than MC from wild type (WT)

mice (p<0.05). After the LPS treatment the expression of costimulatory molecules on

MC was higher than MC from non-treated mice (p<0.05). The expression of CD80 and

CD86 in splenic CD11b+ cells was similar in IL-4 KO and WT. However, after LPS

injections, the expression of MHC class II molecules was also increased in splenic

CD11b+ cells from IL-4 KO mice compared to WT (p<0.05). These preliminary results

suggest that IL-4 may be an important factor modulating CNS inflammatory response in

vivo.