Sacks David, Noben-Trauth Nancy
Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.
Nat Rev Immunol. 2002 Nov;2(11):845-58. doi: 10.1038/nri933.
Established models of T-helper-2-cell dominance in BALB/c mice infected with Leishmania major -- involving the early production of interleukin-4 by a small subset of Leishmania-specific CD4+ T cells -- have been refined by accumulating evidence that this response is not sufficient and, under some circumstances, not required to promote susceptibility. In addition, more recent studies in L. major-resistant mice have revealed complexities in the mechanisms responsible for acquired immunity, which necessitate the redesign of vaccines against Leishmania and other pathogens that require sustained cell-mediated immune responses.
在感染硕大利什曼原虫的BALB/c小鼠中,已建立的辅助性T细胞2型主导模型——涉及一小部分利什曼原虫特异性CD4 + T细胞早期产生白细胞介素-4——已因越来越多的证据而得到完善,这些证据表明这种反应并不充分,并且在某些情况下,对促进易感性而言并非必需。此外,最近在对硕大利什曼原虫具有抗性的小鼠中进行的研究揭示了获得性免疫机制的复杂性,这使得针对利什曼原虫和其他需要持续细胞介导免疫反应的病原体的疫苗需要重新设计。