Schizophrenia is considered a neuropsychiatric syndrome affecting around 1% of the worldwide population. Most typical symptoms are organized in 3 broad categories; positive (delusions, hallucinations), negative (social withdrawal, anhedonia) and cognitive (impaired working memory, attention deficit), genetic and environmental factor are associated with the expression of these symptoms. However, understanding the etiology of schizophrenia symptoms can be challenging due to their heterogeneity.Lately, alterations in the immune system have been linked to the development of schizophrenia, raising the idea of an aberrant cross-talk between the nervous system (NS) and the immune system (IS) in the context of this syndrome. Nevertheless, the precise underlying molecular mechanism of this miscommunication between these two systems is still insufficiently understood. We hypothesize that alterations of two members of the Ikaros family of transcription factors (which are crucial molecules for leukocytes maturation and function) in circulating immune cells play a role in the aberrant communication between these two systems (NS and IS) and contribute to the appearance of the most typical symptoms. We have developed genetical and translational models, combining human samples with mouse models, targeting the communication between the IS and the NS. Our models allowed us to identify gene transcription mechanisms in circulating immune cells and specific secreted molecules that may play a role in the development of schizophrenia-like symptomatology.Based on our results, we propose a model to illustrate the contribution of immune cell secreted molecules to the appearance of schizophrenia-related symptoms.