[Psycho-immunological mechanisms in schizophrenia]

Immune alterations in schizophrenia have been described for decades. Both the unspecific and specific arms of the immune system seem to be involved. Several lines of evidence support that an infectious and/or autoimmune process might play a role in the etiopathogenesis of a group of psychotic disorders. Signs of inflammation and microglia activation in postmortem brains, in the CSF, the dysfunctional Blood Brain Barrier, the increased retroviral activity, the proof of antibodies against brain structures, the signs of T cell activation and the imbalance of cytokine levels in serum, in CSF in in vivo, in vitro and ex vivo conditions, are all strong indicators of the immunological basis of the aetiopathology in schizophrenia. There is a large body of literature aiming at the evaluation of cytokines secreted by different type of cells, not necessarily the immune ones, with the disease being in different states in terms of type of psychosis, course throughout time, type of medication. An inconsistency of the results is common but the majority of the immune alterations favors the hypothesis of activation of the immune system. Furthermore, the immune response of T helper cells in schizophrenia in the literature is characterized by the imbalance between type 1 and type 2, pro-inflammatory and anti-inflammatory respectively, depending on the estimated type of cytokines. The most implicated ones are the IL-1, IL-2, slL-2R, IL-RA, IL-6, slL-6R, IFN, IL-4, IL-10, TNF-alpha and the only quantitave review refutes the current hypothesis of a Th2 slant. On the other hand, it seems that the treatment with antipsychotic drugs affects the cytokine network probably through a shift towards an immune response of Th2-type.