| Background and Objective: Schizophrenia is a severe and common psychiatricdisorder with unknown causation. To understand the etiology and pathogenesis of schizophrenia is one of the most challenging facing the psychiatry field. In many hypotheses regarding the etiology of schizophrenia, the immune dysfunction had always been one of hot spots . Cytokines such as interleukins and tumor necrosis factor alpha(TNF- α ) may play an important role in the etiology and pathogenesis of schizophrenia, in particular TNF- α , there is evidence for a neuroprotective role, but also for a neurotoxic effect on monoamino neurons in various concentrations and influence neural cell growth, proliferation and differentiation. The cytokines may modulate normal brain development in central nervous system. There is some evidence suggesting that cytokines such as TNF- α may affacted neurotransmitters' balance, particular reciprocity with the catecalaminergic system,lead to acute and chronic brain's degeneration. The TNF- α may participated in the pathogenesis of schizophrenia by means of modulating cerebral cortex neuronal number and density. The tumor necrosis factor-beta(TNF- β) also called lymphotoxin-α ,it is a lymphocyte cytokine which play a major role in the immunomodulatory functions. The polymorphism of TNF- β affect the genes express and plasma levels of TNF- β and TNF- α , so the TNF- β gene may also play a role in the pathogenesis of schizophrenia. The TNF- α gene and TNF-β gene are located within the class III region of the major histocompatibility complex(HLAIII) on the short arm of chromosome 6 and are separared by a stretch of approximately 2000 base pairs, a locus associated with genetic susceptibility for schizophrenia; So, the two genes are not only positional but also functional susceptibility genes for schizophrenia. There were some reported that the polymorphism -G308A had been shown to directly affect TNF- α...
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