Lee W M, Holley H P, Stewart J, Galbraith G M
Am J Med Sci. 1986 Jul;292(1):47-52. doi: 10.1097/00000441-198607000-00010.
In a patient with chronic esophageal candidiasis due to C. tropicalis that was refractory to mycostatin and ketoconazole, a generalized cell-mediated immunodeficiency state was detected. Samples of plasma from this patient inhibited T-lymphocyte function, suppressing both rosette formation and mitogen responsiveness of T-cells derived from the patient and from normal individuals. Following plasma exchange, the patient's immune defect resolved and her candida infection disappeared. On further analysis, the plasma inhibitory factor was found to be of low molecular weight (less than 10,000) and heat labile. Preliminary studies suggested that this inhibitor was candida-derived, since it was removed from plasma by anti-candida antibodies in solid phase. Immunodeficiency in chronic candidiasis may be improved by removal of circulating inhibitory factors through plasma exchange.
在一名患有热带念珠菌引起的慢性食管念珠菌病且对制霉菌素和酮康唑治疗无效的患者中，检测到一种全身性细胞介导免疫缺陷状态。该患者的血浆样本抑制T淋巴细胞功能，抑制来自患者和正常个体的T细胞的玫瑰花结形成和丝裂原反应性。血浆置换后，患者的免疫缺陷得到解决，念珠菌感染消失。进一步分析发现，血浆抑制因子分子量低（小于10,000）且热不稳定。初步研究表明，这种抑制剂源自念珠菌，因为它可被固相抗念珠菌抗体从血浆中去除。通过血浆置换去除循环抑制因子，慢性念珠菌病中的免疫缺陷可能会得到改善。
