Dahl M V, Grando S A
Department of Dermatology, University of Minnesota Medical School, Minneapolis.
Adv Dermatol. 1994;9:97-109; discussion 110-1.
T. rubrum is especially suited to survive on the skin surface. We have presented data to show how it accomplishes this. We will now combine these data with our own thoughts to speculate about how T. rubrum has adapted to the skin of human beings. We believe the organism uses several different strategies. First, many infected patients cannot elicit a cell-mediated immune response to eliminate the fungus. The reasons for this are not completely clear, but trichophytin skin tests are negative at 48 hours despite persistent, chronic, and even widespread infections. Antigens are present on T. rubrum, just as they are on other dermatophytes, but differences in antigen penetration through the skin may prevent induction of immunity. Perhaps, neonatal exposure to the fungus or to cross-reacting antigens of molds may induce tolerance by confusing antigen recognition of self vs. nonself. More likely, persistent infection induces immunologic unresponsiveness by activating specific suppressor T cells. In fact, our attempts to clone T. rubrum-specific T cells from peripherals blood have always yielded suppressor cells, and these cells even suppress proliferation of the clone itself. Second, mannans from T. rubrum probably are better able to suppress cell-mediated immune reactions than are mannans from other fungi. T. rubrum may make more mannan than do other dermatophytes, and the mannan may be a more potent immunosuppressor than are mannans from other dermatophytes. Mannan apparently works by inhibiting critical steps in antigen processing or presentation. This inhibits the immune reaction. Perhaps, mannan even can prevent induction under certain circumstances. Third, T. rubrum is not especially aggressive compared with other dermatophytes. By remaining in the stratum corneum, it may evade immune surveillance, and may evade complement and polymorphonuclear leukocytes that would attach the organism if it tried to invade into viable epidermis. Finally, T. rubrum can survive off the human body as a spore. Its life cycle apparently lets spores desquamate and, thereby, remain plentiful in many human habitats. If a spore finds a warm, moist area of skin, it can crowd out normal flora and grow within the stratum corneum. T. rubrum's ability to infect and its ubiquitous presence account for the high incidence of infections. This, plus the ability of T. rubrum to evade host defenses, accounts for the high prevalence of infections with this fungus.
红色毛癣菌特别适合在皮肤表面存活。我们已展示数据来说明它是如何做到这一点的。现在我们将把这些数据与我们自己的想法结合起来，推测红色毛癣菌是如何适应人类皮肤的。我们认为该生物体采用了几种不同的策略。首先，许多受感染的患者无法引发细胞介导的免疫反应来清除真菌。其原因尚不完全清楚，但尽管存在持续、慢性甚至广泛的感染，毛癣菌素皮肤试验在48小时时仍为阴性。红色毛癣菌上存在抗原，就像其他皮肤癣菌一样，但抗原穿透皮肤的差异可能会阻止免疫诱导。也许，新生儿接触真菌或霉菌的交叉反应抗原可能会通过混淆自身与非自身的抗原识别而诱导耐受性。更有可能的是，持续感染通过激活特定的抑制性T细胞诱导免疫无反应性。事实上，我们从外周血中克隆红色毛癣菌特异性T细胞的尝试总是产生抑制细胞，而且这些细胞甚至会抑制克隆自身的增殖。其次，红色毛癣菌的甘露聚糖可能比其他真菌的甘露聚糖更能抑制细胞介导的免疫反应。红色毛癣菌可能比其他皮肤癣菌产生更多的甘露聚糖，并且这种甘露聚糖可能是比其他皮肤癣菌的甘露聚糖更有效的免疫抑制剂。甘露聚糖显然是通过抑制抗原加工或呈递的关键步骤起作用的。这会抑制免疫反应。也许，在某些情况下，甘露聚糖甚至可以阻止免疫诱导。第三，与其他皮肤癣菌相比，红色毛癣菌的侵袭性并不特别强。通过留在角质层中，它可能逃避免疫监视，并且可能逃避补体和多形核白细胞，如果它试图侵入活表皮，这些细胞会附着该生物体。最后，红色毛癣菌可以以孢子的形式在人体外存活。其生命周期显然使孢子脱落，从而在许多人类栖息地中大量存在。如果一个孢子找到温暖、潮湿的皮肤区域，它可以排挤正常菌群并在角质层内生长。红色毛癣菌的感染能力及其无处不在的存在导致了高感染率。这一点，再加上红色毛癣菌逃避宿主防御的能力，导致了这种真菌感染的高患病率。
