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Suppression of In Vitro Lymphocyte Transformation During an Experimental Dermatophyte Infection

机译:实验性皮肤癣菌感染过程中体外淋巴细胞转化的抑制。

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摘要

During primary Trichophyton mentagrophytes infection of strain 2 guinea pigs, the colony-forming units (CFU) of fungi present within the lesion peaked between days 7 and 14, whereas the severity of the lesion itself peaked between days 11 and 16. Concomitant with the latter peak, a pronounced depression in the in vitro mitogenic activity of spleen cells (SPC) and lymph node cells (LNC) was observed. Only after resolution of the primary infection (day 21) did LNC show increased deoxyribonucleic acid (DNA) synthesis in the presence of fungal antigens. During cutaneous reinfection, there was no distinct peak fungal load and CFU appeared to decrease steadily during the accelerated course of a reinfection disease. LNC from guinea pigs with severe, ulcerated reinfection lesions generally exhibited a heightened response to fungal antigen in vitro. LNC from guinea pigs with mild reinfection dermatophytosis had depressed in vitro reactivity to mitogens and dermatophyte antigen. The suppression of blastogenic activity during dermatophyte infection appeared to be associated with autologous serum components, since increased DNA synthesis resulted when SPC or LNC were cultured with fetal calf serum. The depressed in vitro DNA synthesis of lymphocytes (cultured with dermatophyte antigens) that were harvested during reinfection was not accompanied by an impaired ability of infected guinea pigs to respond with a delayed-type hypersensitivity skin test in vivo. These results support the hypothesis that experimental T. mentagrophytes dermatophytosis is a cell-mediated hypersensitivity disease that can be modified by immunosuppressive control mechanisms elaborated or induced by the fungus.
机译:在2型豚鼠的原发毛癣菌感染中,病变内存在的真菌的集落形成单位(CFU)在第7天和第14天之间达到峰值,而病变本身的严重程度则在第11天和第16天之间达到峰值。在峰值时,观察到脾细胞(SPC)和淋巴结细胞(LNC)的体外有丝分裂活性明显降低。仅在原发感染消退后(第21天),在真菌抗原存在下,LNC才显示出脱氧核糖核酸(DNA)合成增加。在皮肤再感染期间,没有明显的峰值真菌负荷,并且在再感染疾病的加速过程中,CFU似乎稳定下降。来自豚鼠的具有严重溃疡再感染病变的LNC在体外通常表现出对真菌抗原的增强反应。来自豚鼠的轻度再感染皮肤癣菌病的LNC在体外对有丝分裂原和皮肤癣菌抗原的反应性降低。皮肤癣菌感染期间抑制成胚活性似乎与自体血清成分有关,因为当用胎牛血清培养SPC或LNC时,DNA合成增加。再感染过程中收获的淋巴细胞(与皮肤癣菌抗原一起培养)体外DNA合成的抑制并不伴随着被感染豚鼠对体内迟发型超敏反应皮肤试验的反应能力受损。这些结果支持这样的假设,即实验性毛囊癣菌皮肤癣菌病是一种细胞介导的超敏性疾病,可以通过由真菌阐明或诱导的免疫抑制控制机制加以修饰。

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