Melby P C, Andrade-Narvaez F, Darnell B J, Valencia-Pacheco G
Department of Medicine, University of Texas Health Science Center, San Antonio, USA.
FEMS Immunol Med Microbiol. 1996 Sep;15(2-3):101-7. doi: 10.1111/j.1574-695X.1996.tb00059.x.
Th1-type cellular immune responses (interferon-gamma) play a critical role in protection against Leishmania spp. infection, whereas Th2-type cytokines (interleukin (IL)-4, IL-10) have a counter-protective effect. IL-12, a potent inducer of Th1-type cellular immune responses, may play a pivotal role in the development of a protective response. We found that IL-10 and IL-12 mRNAs were expressed in most lesions of individuals with active cutaneous leishmaniasis. The quantity of IL-12 mRNA was highly variable but correlated strongly with the level of interferon-gamma expression. IL-12 expression also paralleled the expression of IL-10, a potent in vitro suppressor of IL-12 and interferon-gamma production. The more chronic, non-healing lesions generally had higher levels of IL-12 mRNA indicating that the expression of this cytokine alone was not sufficient to induce healing. Although the in situ production of IL-10 did not appear to block IL-12 expression, IL-10 may still promote disease by direct suppression of macrophage activation.
1型辅助性T细胞（Th1）介导的细胞免疫反应（γ干扰素）在抵抗利什曼原虫感染中起关键作用，而2型辅助性T细胞（Th2）细胞因子（白细胞介素（IL）-4、IL-10）则具有反保护作用。IL-12是Th1型细胞免疫反应的强效诱导剂，可能在保护性反应的发展中起关键作用。我们发现，IL-10和IL-12信使核糖核酸（mRNA）在活动性皮肤利什曼病患者的大多数皮损中表达。IL-12 mRNA的量变化很大，但与γ干扰素的表达水平密切相关。IL-12的表达也与IL-10的表达平行，IL-10在体外是IL-12和γ干扰素产生的强效抑制剂。病程更长、不愈合的皮损通常IL-12 mRNA水平更高，这表明仅这种细胞因子的表达不足以诱导愈合。虽然IL-10的原位产生似乎并未阻断IL-12的表达，但IL-10仍可能通过直接抑制巨噬细胞活化来促进疾病发展。
