Superantigen-like effects of a Candida albicans polypeptide
Superantigen-like effects of a Candida albicans polypeptide
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DOI：
10.1086/529203
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发表时间：
2008-04-01
影响因子：
6.4
通讯作者：
Hostetter, Margaret K.
中科院分区：
文献类型：
--
作者：
Devore-Carter, Denise;Kar, Sujata;Hostetter, Margaret K.
白色念珠菌细胞壁蛋白 Int1 的氨基末端序列与关节炎支原体超抗原 MAM 的主要组织相容性复合体 (MHC) II 类结合位点表现出部分同一性。 Int1 阳性白色念珠菌芽生孢子激活人 T 淋巴细胞并扩增 V β 亚群 2、3 和/或 14； Int1阴性菌株没有活性。干扰素-γ (IFN-gamma) 的释放但肿瘤坏死因子-α 或白介素-6 的释放不依赖于 Int1；未检测到白细胞介素 4 和白细胞介素 10。 T 淋巴细胞激活、V beta 扩增和 IFN-γ 释放与包含 Int1 前 263 个氨基酸的可溶性多肽 (Pep(263)) 相关。单克隆抗体 163.5 识别与 MAM 同一区域重叠的 Int1 表位，当由 Int1 阳性芽生孢子或 Pep(263) 触发时显着抑制这些活性，但不由葡萄球菌肠毒素 B 触发。需要组氨酸 (263)。 Pep(263) 与 T 淋巴细胞和 MHC II 类结合，并在白色念珠菌真菌血症患者的尿液中检测到。这些研究鉴定出一种具有超抗原样活性的念珠菌蛋白。
The amino terminal sequence of the Candida albicans cell wall protein Int1 exhibited partial identity with the major histocompatibility complex ( MHC) class II binding site of the Mycoplasma arthritidis superantigen MAM. Int1-positive C. albicans blastospores activated human T lymphocytes and expanded V beta subsets 2, 3, and/or 14; Int1-negative strains were inactive. Release of interferon-gamma ( IFN-gamma) but not of tumor necrosis factor-alpha or interleukin-6 was Int1 dependent; interleukin-4 and interleukin-10 were not detected. T lymphocyte activation, V beta expansion, and IFN-gamma release were associated with a soluble polypeptide that encompassed the first 263 amino acids of Int1 ( Pep(263)). Monoclonal antibody 163.5, which recognizes an Int1 epitope that overlaps the region of identity with MAM, significantly inhibited these activities when triggered by Int1-positive blastospores or Pep(263) but not by staphylococcal enterotoxin B. Histidine(263) was required. Pep(263) bound to T lymphocytes and MHC class II and was detected in the urine of a patient with C. albicans fungemia. These studies identify a candidal protein that displays superantigen-like activities.