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Catholic University of Daegu, College of Natural Sciences, Dept. Occupational Health, Gyeongbuk, Korea*The Catholic University of Korea, College of Medicine, Dept. Preventive Medicine, Seoul, KoreaABSTRACTObjectives: This study was undertaken in order to evaluate a potential mechanism involved in gastro-intestinalproblems observed in autistic subjects and uses an animal model of autism investigation.Methods: BTBR T+tf/J, a mouse strain with typical socio-behavioral characteristics of autistic subjects and FVBmice with highly social behaviors as the control strain were used. Both genders of mice aged three weeks and sixmonths were used from four separate litters for each strain. Serum was prepared following cardiac puncture, andmesenteric lymph nodes were collected for in vitro stimulation and enumeration of major immune cell proportion. Results: The level of serum IgA was significantly enhanced in six-month-old BTBR mice compared with three-week-old BTBR, which was not observed with the FVB control mice. The serum IgE level was also higheramong BTBR mice than among age-sex matched FVB mice, respectively. Considering the ratio of interleukin-4 vs interferon-gamma production from mesenteric lymph node T cells, skewedness toward type-2 reactivitieswas observed. In addition, the proportion of B cells in mesenteric lymph nodes was significantly higher in BTBRmice than in FVB mice. Conclusion: Upregulation of mucosal immunity related with enhanced type-2 immune reactivity observed inBTBR mice could be involved with the etiology of gastro-intestinal abnormalities in autism.Keywords: autism, mucosal immunity, BTBR T+tf/J mice, IgA |
