Perskvist Nasrin, Skoglund Karin, Edston Erik, Bäckström Gerd, Lodestad Iréne, Palm Ulla
National Board of Forensic Medicine, Department of Forensic Medicine, Linköping Division, Linköping , Sweden.
Fetal Pediatr Pathol. 2008;27(3):149-65. doi: 10.1080/15513810802077651.
We hypothesized that genetic variations of cytokines could contribute to the risk of developing a fatal immunological reaction in the heart of infants. Thus, tumor necrosis factor (TNF)-alpha and interleukin (IL)-10 gene polymorphisms versus induction of cardioimmunologxical responses in victims of sudden infant death syndrome (SIDS) were explored. We genotyped 35 infants (23 cases of SIDS and 12 infants with a known cause of death), and 100 healthy adult controls for IL-10 -1082 G/A, -592 C/A and TNF-alpha-238 G/A, -308 G/A. We found a higher frequency of the ATA haplotype and ATA/ATA genotype of IL-10 associated with SIDS (13%). The frequency of homozygote infants for IL-10 haplotypes in SIDS was higher (52%) than the control group (34%). All SIDS cases were homozygotice for the TNF-alpha-238 G allele and 20 infants were homozygous for the TNF-alpha-308 G allele in the same group. None of the infants with higher levels of infiltrated T-cells (n=8) was homozygous for IL-10 gene polymorphisms, whereas in contrast 3 cases of the 6 that displayed higher levels of cardiac mast cells were homozygous. In this study, the increased number of interstitial T-cells, mast cells, and macrophages in the myocardial interstitium demonstrated no correlation with the genotype for either cytokines.
我们推测,细胞因子的基因变异可能会增加婴儿发生致命性心脏免疫反应的风险。因此,我们探究了肿瘤坏死因子(TNF)-α和白细胞介素(IL)-10基因多态性与婴儿猝死综合征(SIDS)受害者心脏免疫反应诱导之间的关系。我们对35名婴儿(23例SIDS和12例已知死因的婴儿)以及100名健康成人对照进行了IL-10 -1082 G/A、-592 C/A和TNF-α -238 G/A、-308 G/A基因分型。我们发现,与SIDS相关的IL-10的ATA单倍型和ATA/ATA基因型频率更高(13%)。SIDS中IL-10单倍型纯合子婴儿的频率(52%)高于对照组(34%)。在同一组中,所有SIDS病例的TNF-α -238 G等位基因均为纯合子,20名婴儿的TNF-α -308 G等位基因也为纯合子。浸润性T细胞水平较高的婴儿(n = 8)中,没有一例IL-10基因多态性为纯合子,而在心脏肥大细胞水平较高的6例婴儿中,有3例为纯合子。在本研究中,心肌间质中间质T细胞、肥大细胞和巨噬细胞数量的增加与两种细胞因子的基因型均无相关性。