Humoral and cellular immune recognition of Helicobacter pylori proteins are not concordant.
Humoral and cellular immune recognition of Helicobacter pylori proteins are not concordant.
复制标题
幽门螺杆菌蛋白的体液免疫和细胞免疫识别不一致。
DOI：
10.1111/j.1365-2249.1994.tb06590.x
复制
发表时间：
1994
影响因子：
4.6
通讯作者：
Blaser,MJ
中科院分区：
文献类型：
--
作者：
Sharma,SA;Miller,GG;Perez-Perez,GI;Gupta,RS;Blaser,MJ
幽门螺杆菌是慢性胃窦性炎和消化性溃疡的主要病因。需要进一步定义决定受感染个体是否保持无症状，或最终发展为粘膜溃疡或转化为恶性肿瘤的因素。探讨宿主对h反应的可能性。幽门菌可能在这种感染的结果中起作用。我们已经检查了几种h的体液和细胞识别。血清阳性和血清阴性的幽门蛋白。水可提取细胞蛋白的复杂混合物，不包括脂多糖（LPS），仅在血清阳性或感染个体中被血清抗体识别。来自血清阳性受试者的IgG也与脲酶和与65‐kD分枝杆菌热休克蛋白同源的热休克蛋白（hsp）60结合，而来自未感染个体的血清则为阴性。尽管对这些抗原的抗体反应仅限于血清阳性受试者，但在血清阳性和血清阴性受试者中都发现了对相同蛋白质的T细胞识别。h。幽门刺激所有受试者的外周血单核细胞（PBMC），而纯化蛋白仅激活部分血清阳性和血清阴性受试者的淋巴细胞。被h激活的PBMC。pyloorihsp60对自体人p60热休克蛋白无应答。这些结果表明，与抗体反应相反，T细胞对h。幽门蛋白可能出现在未感染者身上。此外，数据表明，在这些受试者中，被细菌热休克蛋白激活的外周淋巴细胞不会通过识别人类热休克同源物来介导组织损伤。
Helicobacter pyloriis a major cause of chronic antral gastritis and peptic ulcer disease. Further definition is needed of the factors that determine whether infected individuals remain asymptomatic, or ultimately develop ulceration of the mucosa or transformation to malignancy. To explore the possibility that host response toH. pylorimay play a role in the outcome of this infection. we have examined humoral and cellular recognition of severalH. pyloriproteins by seropositive and seronegative persons. A complex mixture of water‐extractable cell proteins, which did not include lipopolysaccharide (LPS), was recognized by serum antibodies only in seropositive or infected individuals. IgG from seropositive subjects also bound to urease and to a heat shock protein (hsp)60 that is homologous to the 65‐kD mycobacterial heat shock protein, while sera from uninfected individuals were negative. Although antibody responses to these antigens were restricted to seropositive subjects, T cell recognition of the same proteins was found in both seropositive and seronegative subjects. The water extract ofH. pyloristimulated peripheral blood mononuclear cells (PBMC) from all subjects, while purified proteins activated lymphocytes of only some seropositive and seronegative subjects. PBMC that were activated by theH. pylorihsp60 did not respond to the autologous human p60 heat shock protein. These results demonstrate that, in contrast to antibody responses, T cell recognition ofH. pyloriproteins may occur in non‐infected persons. In addition, the data suggest that in these subjects, peripheral lymphocytes that are activated by bacterial heat shock proteins do not mediate tissue damage by recognition of human heat shock homologues.