Mohr David C, Genain Claude
Departments of Psychiatry and Neurology, and VA Medical Center, University of California-San Francisco, 4150 Clement Street (116-A), San Francisco, CA 94121, USA.
J Psychosom Res. 2004 Aug;57(2):155-8. doi: 10.1016/S0022-3999(03)00601-9.
This study examined the buffering effects of social support on the relationship between depression and autoaggressive immune function in multiple sclerosis (MS).
Fourteen participants with comorbid diagnoses of MS and major depressive disorder received 16 weeks of psychotherapy or antidepressant medications. Depression and T-cell production of interferon-gamma (IFN-gamma), a lynchpin in MS pathogenesis, were assessed at baseline and posttreatment. Social support was assessed at baseline.
Both depression and T-cell production of IFN-gamma were significantly reduced over the 16 weeks of treatment. There was a significant interaction between change in depression, change in IFN-gamma, and social support (R(2)=.26, P=.03) such that social support served as a buffer.
These results support the hypothesis that social support buffers the effects of change in depression on IFN-gamma production. However, these findings should be viewed as preliminary due to the small sample size and the absence of a control condition.
本研究探讨了社会支持对多发性硬化症(MS)患者抑郁与自身攻击性免疫功能之间关系的缓冲作用。
14名患有MS合并重度抑郁症的参与者接受了16周的心理治疗或抗抑郁药物治疗。在基线和治疗后评估抑郁情况以及T细胞产生γ-干扰素(IFN-γ)的情况,IFN-γ是MS发病机制中的关键因素。在基线时评估社会支持情况。
在16周的治疗过程中,抑郁和T细胞产生IFN-γ的情况均显著改善。抑郁变化、IFN-γ变化和社会支持之间存在显著交互作用(R(2)=.26,P=.03),表明社会支持起到了缓冲作用。
这些结果支持了社会支持缓冲抑郁变化对IFN-γ产生影响的假设。然而,由于样本量小且缺乏对照条件,这些发现应被视为初步结果。