Blanco Jose L, Garcia Marta E
Departamento Sanidad Animal, Facultad de Veterinaria, Universidad Complutense, 28040 Madrid, Spain.
Vet Immunol Immunopathol. 2008 Sep 15;125(1-2):47-70. doi: 10.1016/j.vetimm.2008.04.020. Epub 2008 May 9.
The immune mechanisms of defence against fungal infections are numerous, and range from protective mechanisms that were present early in evolution (innate immunity) to sophisticated adaptive mechanisms that are induced specifically during infection and disease (adaptive immunity). The first-line innate mechanism is the presence of physical barriers in the form of skin and mucous membranes, which is complemented by cell membranes, cellular receptors and humoral factors. There has been a debate about the relative contribution of humoral and cellular immunity to host defence against fungal infections. For a long time it was considered that cell-mediated immunity (CMI) was important, but humoral immunity had little or no role. However, it is accepted now that CMI is the main mechanism of defence, but that certain types of antibody response are protective. In general, Th1-type CMI is required for clearance of a fungal infection, while Th2 immunity usually results in susceptibility to infection. Aspergillosis, which is a disease caused by the fungus Aspergillus, has been the subject of many studies, including details of the immune response. Attempts to relate aspergillosis to some form of immunosuppression in animals, as is the case with humans, have not been successful to date. The defence against Aspergillus is based on recognition of the pathogen, a rapidly deployed and highly effective innate effector phase, and a delayed but robust adaptive effector phase. Candida albicans, part of the normal microbial flora associated with mucous surfaces, can be present as congenital candidiasis or as acquired defects of cell-mediated immunity. Resistance to this yeast is associated with Th1 CMI, whereas Th2 immunity is associated with susceptibility to systemic infection. Dermatophytes produce skin alterations in humans and other animals, and the essential role of the CMI response is to destroy the fungi and produce an immunoprotective status against re-infection. The resolution of the disease is associated with a delayed hypersensitive response. There are many effective veterinary vaccines against dermatophytoses. Malassezia pachydermatis is an opportunistic yeast that needs predisposing factors to cause disease, often related to an atopic status in the animal. Two species can be differentiated within the genus Cryptococcus with immunologic consequences: C. neoformans infects predominantly immunocompromised hosts, and C. gattii infects non-immunocompromised hosts. Pneumocystis is a fungus that infects only immunosupressed individuals, inducing a host defence mechanism similar to that induced by other fungal pathogens, such as Aspergillus.
抵御真菌感染的免疫机制多种多样,从进化早期就存在的保护机制(固有免疫)到感染和疾病期间特异性诱导产生的复杂适应性机制(适应性免疫)。第一道固有防线是皮肤和黏膜形式的物理屏障,细胞膜、细胞受体和体液因子对其起到补充作用。关于体液免疫和细胞免疫在宿主抵御真菌感染中的相对贡献一直存在争议。长期以来,人们认为细胞介导免疫(CMI)很重要,但体液免疫作用很小或没有作用。然而,现在人们公认CMI是主要的防御机制,但某些类型的抗体反应也具有保护作用。一般来说,清除真菌感染需要Th1型CMI,而Th2免疫通常会导致易感性增加。曲霉病是由曲霉菌引起的疾病,它一直是许多研究的对象,包括免疫反应的细节。迄今为止,试图将动物中的曲霉病与某种形式的免疫抑制联系起来(就像人类的情况一样)尚未成功。对曲霉的防御基于对病原体的识别、迅速部署且高效的固有效应阶段以及延迟但强大的适应性效应阶段。白色念珠菌是与黏膜表面相关的正常微生物群落的一部分,可表现为先天性念珠菌病或细胞介导免疫的后天缺陷。对这种酵母菌的抵抗力与Th1 CMI相关,而Th2免疫与全身感染的易感性相关。皮肤癣菌会在人类和其他动物身上引起皮肤病变,CMI反应的重要作用是破坏真菌并产生针对再次感染的免疫保护状态。疾病的消退与迟发型超敏反应相关。有许多有效的兽用疫苗可用于防治皮肤癣菌病。厚皮马拉色菌是一种机会性酵母菌,需要诱发因素才能致病,这些因素通常与动物的特应性状态有关。新型隐球菌属内有两个物种具有免疫方面的差异:新生隐球菌主要感染免疫功能低下的宿主,而格特隐球菌感染免疫功能正常的宿主。肺孢子菌是一种仅感染免疫抑制个体的真菌,其诱导的宿主防御机制与其他真菌病原体(如曲霉)诱导的机制相似。