LAUSR

In this issue of BBI Melbourne et al describe a reduced activity of the JAK-STAT1 pathway in leukocytes of early and acute schizophrenia patients. This editorial discusses the report of Melbourne et al as being in accord with the view that active forms of schizophrenia are characterized by a de-activation of the Th1 driven M1/JAK-STAT1 mediated pro-inflammatory pathway in myeloid cells (macrophages, dendritic cells and microglia). Myeloid cells can be inflammatory activated and de-activated via various different molecular pathways (leading to various types of macrophages, such as e.g. various M1, various M2 and atherosclerosis related macrophages). There are data in the literature that pathways related to the Th17 driven MAP-kinase pro-inflammatory M1 pathway are activated in the myeloid cells of early and acute schizophrenia. The question thus arises what the intracellular molecular processes are which drive the complex inflammatory set points of macrophages and microglia in early and acute forms of schizophrenia.