Immunological hypothesis of schizophrenia, more than a hundred-year-old theory, has been in very focus of modern science for the last twenty years. The aim of this paper was to review and systematize current findings on neuroinflammation as schizophrenia etiology. In order to find relevant literature, PubMed/MEDLINE, Clinical Key and Science Direct databases were searched by Medical Subject Headings (MeSH) and other keywords (such as “schizophrenia“, “immunology“, “neuroinflammation“, etc.). Based on recent literature from psychoneuroimmunology field, the review on immunological aspect of schizophrenia etiology was given, and diagnostic inflammation biomarkers, as well as possible antiinflammatory adjuvant therapy, were suggested. Immunological hypothesis of schizophrenia is in line with the stress-diathesis model – a theory suggesting that schizophrenia originates in genetically suspectible individuals or due to repetead stress during the vulnerable period that results in activation of inadequate immunological response which leads to morphological changes of the brain, neurochemical disbalance, and lastly, specific psychopathology. Perplexity of schizophrenia research lies in substantial inconsistency of study results owing to the heterogeneity of the disease. Nevertheless, if those schizophrenia etiology hypotheses were true, inflammation biomarkers could contribute to objectivity and be of great use in the diagnostic process. Moreover, a plethora of antiinflammatory drugs already on the market (NSAIDs, COX-2 inhibitors, omega-3 fatty acids, etc.) could be added to antipsychotics as adjuvant therapy. In conclusion, it's possible that inflammation is a background process is only one of many schizophrenia subtypes.