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The Th1/Th2-like switch in syphilitic infection: is it detrimental?

机译：梅毒感染中类似Th1 / Th2的开关：是否有害？

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Organisms that cause chronic diseases have evolved mechanisms to evade those immune defenses that resolve the acute stage of infection (10, 12-14, 21, 22, 32, 35, 37, 38, 40, 42, 45-49, 53). Much is to be learned by specifically identifying the mechanisms underlying these evasive strategies. Important new insights will emerge in terms of immunoregulatory pathways. This in turn will facilitate vaccine development. A good example is leishmania infection. The acute stage of this disease is resolved by DTH-macrophage activation. Leishmanial components preferentially activate Th2 lymphocytes. As a consequence, Th1 effects are minimized and infection is exacerbated leading to chronicity (10, 14, 32). To overcome this negative tendency, leishmanial vaccines are administered in combination with exogenous gamma interferon (42). This selects for Th1 predominance and generates protective immunity. Syphilis exhibits many parallels to the other nine chronic diseases mentioned above. Similarities include an acute localized stage that readily heals, early clearance via DTH-macrophage activation, transient concomitant immunity during acute infection, development of macrophage suppression through PGE2 down-regulation, beneficial effects of exogenous gamma interferon, and elements of autoimmunity. Some of the complexities of immunoregulation during treponemal infection have just begun to be unraveled. It will be important to develop further insight into the Th1/Th2 switch especially as it relates to chronicity. Macrophages seem to be intimately involved in the mechanics of this switch, and their specific role needs further clarification. Whatever is learned about syphilis, as well as other chronic infections will contribute to a better understanding of the generalized pathways of immunoregulation.
机译：导致慢性疾病的生物已经进化出逃避解决急性感染阶段的免疫防御的机制（10、12-14、21、22、32、35、37、38、40、42、45-49、53）。通过专门确定这些规避策略的机制，可以学到很多东西。重要的新见解将在免疫调节途径方面出现。反过来，这将有助于疫苗的开发。一个很好的例子是利什曼原虫感染。该疾病的急性期通过DTH-巨噬细胞活化而解决。利什曼成分优先激活Th2淋巴细胞。结果，Th1的作用降到最低，感染加剧，导致慢性（10、14、32）。为了克服这种负面趋势，利什曼疫苗与外源性γ干扰素联合使用（42）。这将选择Th1优势并产生保护性免疫。梅毒与上述其他九种慢性疾病有许多相似之处。相似之处包括易于治愈的急性局限期，通过DTH-巨噬细胞活化而早期清除，在急性感染期间的瞬时伴随免疫，通过PGE2下调产生巨噬细胞抑制作用，外源性γ干扰素的有益作用以及自身免疫因素。刚刚揭开了在耳蜗感染期间免疫调节的一些复杂性。重要的是进一步了解Th1 / Th2开关，尤其是与慢性有关的开关。巨噬细胞似乎与这种转换机制密切相关，它们的具体作用需要进一步阐明。无论对梅毒以及其他慢性感染有何了解，都将有助于人们更好地了解免疫调节的一般途径。

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