Serum levels of macrophage migration inhibitory factor in children and adolescents with autistic disorders

ABSTRACT

There is growing awareness of an immunological involvement in children with autistic disorder [AD]. Studies suggest that innate rather than adaptive neuroimmune responses are associated with autism. Macrophage migration inhibitory factor [MIF], being an upstream regulator of innate and adaptive immunity, could play a role in this disorder. We aimed to study serum levels of MIF in a subset of children with autism and its relation to disease severity and important clinical manifestations of the disease. The study included 21 children and adolescents diagnosed with AD with a mean age of 6.9 +/- 2.9 years. Patients were neurologically evaluated and categorized into those with mild to moderate autism and those with severe disorder. In addition to assessment of cognitive abilities and electroencephalogram performance, MIF levels were measured in the sera of included patients and were compared to those of a matched control group. Levels of MIF were not significantly different in the patients and the control group. However, serum MIF was significantly reduced in patients with severe AD [z=2. 197, P=0. 029] compared to those with milder disease. Furthermore, there was a significant negative correlation between MIF levels and the degree of severity of the non-verbal communicative skills [r=-0.49, P=0. 042]. MJF levels were not different in patients with mental retardation, or abnormal electroencephalogram when compared to the rest of the patients. Our study suggests the presence of immune dysfunction in the form of derangement in serum MIF levels in children with AD. Its levels were specifically decreased in a subset of patients with severe disorder compared to those with mild to moderate disease. Decreased serum levels of MIF in patients with AD seem to be associated with worsening of the nonverbal communicative skills which is one of the disturbed behavioral parameters of AD. Further research is warranted to study the precise relationship of immune derangement and both the etiopathogenesis and the behavioral components of AD and its therapeutic implications