CONICET | Buscador de Institutos y Recursos Humanos

Background: Several studies indicate that dopamine plays a role in the interaction between the nervous and immune systems. Dopamine, by an inhibitory tone, regulates prolactin secretion by the hypophyseal lactotroph cells, which in turn could modulate immune cells. Furthermore, it has been reported that some patients with autoimmune diseases course with hiperprolactinemia. In this study, we investigated whether dopamine receptor antagonism modulates experimental autoimmunity.Methods: Chronic dopamine receptor antagonism was performed by daily intraperitoneal administration of eticlopride (Eti) in type-1 diabetes mice (NODn=9) from month 3 to 7. Control mice(n=8) were injected with PBS. Disease severity was evaluated by the assessment of survival, glucosuria, spleen cell expansion and leukocyte infiltration of the pancreas.Results: Interestingly, we found that chronic dopamine receptor antagonism decreased survival rate compared with untreated (UT) mice (UT 87,5% (7/8) vs Eti 55%(5/9)). Eti administration increased incidence of glucosuria (UT 25% (2/8) vs Eti 66,6%(6/9)). Furthermore, Eti treated group showed a 2,6 fold increase in leukocyte infiltration of the pancreas measured by FACS. Spleen weight in Eti treated mice was greater than in UT mice (UT 125±10 vs Eti 177±16 mg;p=0,0184). Although total CD3+ CD4+ T cells from spleen were increased in the Eti treated mice (UT 39,7±3,0 vs Eti 48,0±1,0%;p=0,0393), no changes were observed in CD8+ or activated CD69+ T cell populations. Although further research needs to be done, our data support the notion that dopamine and dopamine receptor axis play a crucial role in autoimmune progression, promoting this axis as a target for new immunotherapies design.