Theodos C M
Division of Infectious Diseases, Tufts University School of Veterinary Medicine, North Grafton, MA 01536, USA.
Adv Parasitol. 1998;40:87-119. doi: 10.1016/s0065-308x(08)60118-9.
Cryptosporidium parvum has gained much attention as a major cause of diarrhea in the world. Knowledge of the host immune mechanisms responsible for the clearance of this parasite from the gastrointestinal tract may prove to be vital for successful therapeutic treatment of cryptosporidiosis, particularly in the immunodeficient host. This chapter focuses on the innate and cell-mediated immune mechanisms associated with resistance to and resolution of a C. parvum infection. Much of the work in these areas is still in its infancy. Despite this, general consensus supports a role for interferon-gamma (IFN gamma) in mediating the initial resistance to C. parvum, although the mechanism by which this cytokine imparts resistance is unclear. It is also generally agreed that CD4+ T lymphocytes are required for the resolution of both acute and chronic cryptosporidiosis. However, the effector mechanism is again unclear. Several studies suggest that IFN gamma may also be involved in the resolution of cryptosporidiosis. However, the extent to which this cytokine is involved in the actual resolution of infection has been debated. Less extensive studies investigating the participation of other cells and cytokines in the innate and cell-mediated immune responses to C. parvum are also discussed.
微小隐孢子虫作为全球腹泻的主要病因已备受关注。了解负责从胃肠道清除这种寄生虫的宿主免疫机制,可能对隐孢子虫病的成功治疗至关重要,尤其是在免疫缺陷宿主中。本章重点关注与抵抗和清除微小隐孢子虫感染相关的固有免疫和细胞介导免疫机制。这些领域的许多工作仍处于起步阶段。尽管如此,普遍共识支持干扰素-γ(IFNγ)在介导对微小隐孢子虫的初始抵抗中发挥作用,尽管这种细胞因子赋予抵抗力的机制尚不清楚。人们还普遍认为,急性和慢性隐孢子虫病的消退都需要CD4 + T淋巴细胞。然而,效应机制同样不明确。多项研究表明,IFNγ可能也参与隐孢子虫病的消退。然而,这种细胞因子在感染实际消退中的参与程度一直存在争议。还讨论了较少的关于其他细胞和细胞因子参与对微小隐孢子虫固有免疫和细胞介导免疫反应的研究。