Decreased Expression of CD95 (FAS/APO-1) on CD4+ T-lymphocytes from Participants with Autism |
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Authors: | Henrik A. Engstrom Sten Ohlson E. Gene Stubbs Alma Maciulis Virgil Caldwell J. Dennis Odell Anthony R. Torres |
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Affiliation: | (1) Department of Chemistry and Biomedical Sciences, University of Kalmar, Kalmar, Sweden;(2) Child Development and Rehabilitation Center, University of Oregon, Portland, Oregon;(3) Center for Persons with Disabilities, Biology Department, Utah State University, Logan, Utah |
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Abstract: | Although autism remains an enigmatic disease, there is mounting evidence that the immune system plays an important role in the pathogenesis. Immune system involvement is apparently widespread as numerous humoral and cellular abnormalities have been reported in both the innate and adaptive responses. Fas (CD95/APO-1) is a type I cell-surface protein from the TNF/NGF-R superfamily present on the surface of many immune related cells. Fas activation is instrumental in starting a complicated chain of events that results in programmed cell death (apoptosis) by DNA fragmentation. Preliminary data is presented, which indicate that subjects with austism have lower levels of Fas on their CD4+ helper T cells (p = .048) than have normal subjects. Data also indicates subjects with autism have significantly higher levels of soluble Fas (p = .01) than have normal subjects. A maturing individual must eliminate cells for proper morphogenesis to occur. Preliminary data suggest that faulty apoptosis may be involved in the pathogenesis of autism. |
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Keywords: | autism apoptosis FAS CD95 APO-1 |
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