Helgeland L, Tysk C, Järnerot G, Kett K, Lindberg E, Danielsson D, Andersen S N, Brandtzaeg P
Laboratory for Immunohistochemistry and Immunopathology, (LIIPAT), University of Oslo, National Hospital, Norway.
Gut. 1992 Oct;33(10):1358-64. doi: 10.1136/gut.33.10.1358.
Serum samples from 26 monozygotic twin pairs concordant or discordant with regard to inflammatory bowel disease, and rectal biopsies from 42 twins of the same subject group, were examined for IgG subclasses. They were all compared with normal controls. Almost all affected twins were in clinical remission. Paired immunofluorescence staining of the rectal mucosa showed that those with ulcerative colitis had a significantly higher (p < 0.01) proportion of IgG1 producing mucosal immunocytes than normal controls (78.1% v 55.9%). Conversely, the IgG2 cell fraction was significantly reduced (15.9% v 34.6%). Healthy twins from ulcerative colitis pairs tended to show a raised proportion of IgG1 cells and the IgG2 cell fraction was significantly reduced (p < 0.05). In discordant ulcerative colitis twin pairs, no difference appeared in the cellular IgG subclass pattern between healthy and affected twins. Furthermore, the proportion of IgG1 in these healthy and diseased twins showed good correlation (T = 0.867). The results in rectal mucosa of twins with Crohn's disease were widely scattered and affected twins did not differ significantly from normal controls. Healthy twins, however, showed a marginally raised IgG1 cell proportion, but no correlation was seen between the IgG subclass fractions in discordant Crohn's disease twin pairs. The serum concentrations of IgG1 and IgG2 did not differ from normal controls in twins of either category. These results suggested that in ulcerative colitis, the aberrant mucosal production of IgG1 and IgG2 does not depend on active disease, but is apparently at least partially explained by a genetic impact. Conversely, the mucosal IgG subclass pattern in Crohn's disease appears to be determined mainly by exogenous variables.
对26对在炎症性肠病方面一致或不一致的同卵双胞胎的血清样本，以及来自同一受试组的42对双胞胎的直肠活检样本进行了IgG亚类检测。将它们与正常对照组进行了比较。几乎所有患病双胞胎都处于临床缓解期。直肠黏膜的配对免疫荧光染色显示，溃疡性结肠炎患者产生IgG1的黏膜免疫细胞比例显著高于正常对照组（p<0.01）（78.1%对55.9%）。相反，IgG2细胞比例显著降低（15.9%对34.6%）。溃疡性结肠炎双胞胎对中的健康双胞胎倾向于显示IgG1细胞比例升高，且IgG2细胞比例显著降低（p<0.05）。在不一致的溃疡性结肠炎双胞胎对中，健康双胞胎和患病双胞胎的细胞IgG亚类模式没有差异。此外，这些健康和患病双胞胎中IgG1的比例显示出良好的相关性（T=0.867）。克罗恩病双胞胎的直肠黏膜检测结果差异很大，患病双胞胎与正常对照组没有显著差异。然而，健康双胞胎的IgG1细胞比例略有升高，但在不一致的克罗恩病双胞胎对中，IgG亚类比例之间没有相关性。两类双胞胎的血清IgG1和IgG2浓度与正常对照组没有差异。这些结果表明，在溃疡性结肠炎中，IgG1和IgG2的异常黏膜产生不依赖于活动性疾病，显然至少部分是由遗传影响所致。相反，克罗恩病中的黏膜IgG亚类模式似乎主要由外源性变量决定。
