Decreased Interferon Production in Schizophrenic Patients

Moises, Hans W.; Beck, J; Schindler, L.; Kirchner, H.

doi:10.1055/s-2007-1017207

Cited by 7 publications

(1 citation statement)

References 3 publications

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“…Several studies of interferon in schizophrenia patients have reported no change in interferon concentrations or a decrease in interferon production by cultured lymphocytes (Rimon et al 1983(Rimon et al , 1985Moises et al 1985Moises et al , 1986Roy et al 1985;Schindler et al 1986;Ahokas et al 1987;). There is one report of increased serum interferon concentrations in a subgroup of schizophrenia patients who appeared to have more prominent psychotic symptoms (Preble and .…”

Section: Markers Of Immune Activationmentioning

confidence: 99%

Infection and Autoimmunity as Etiologic Factors in Schizophrenia: A Review and Reappraisal

Kirch

1993

Schizophrenia Bulletin

164

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The focus of schizophrenia research has been turning from studies of structural and functional brain abnormalities to an increasing emphasis on possible etiologic factors. One etiologic hypothesis is that schizophrenia is the result of an infection (especially by a virus) or of an autoimmune reaction (perhaps following an infection) against central nervous system (CNS) tissue. Indirect evidence supporting this hypothesis includes possible geographic variance in the prevalence of schizophrenia, a season-of-birth effect, and observed associations between schizophrenia and prenatal exposure to viral epidemics. Several studies of cell-based and humoral immunity, as well as studies of cytokines, have indicated abnormalities in the immune function of schizophrenia patients, but many of these findings have not been replicated consistently. In addition, most observed alterations in immune function have been modest in degree and nonspecific. Attempts to identify a specific infectious agent or an antibody directed against CNS tissue have not produced a consistently replicable finding. In summary, no research evidence to date irrefutably indicates an infectious or autoimmune etiologic process in schizophrenia. It is probably unreasonable, however, to view schizophrenia as having a single cause. It is much more likely to be a heterogeneous disorder resulting from interactions between multiple factors, including the person's genetic endowment and various environmental influences. Infectious agents or CNS autoantibodies may well be among these environmental variables. A major current emphasis is on studying potential interactions between exposure to an infection or an autoimmune response and key early phases of brain development. A corresponding priority in the research agenda will be the development of animal models of CNS development that might elucidate the pathogenic mechanisms of such an interaction.

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