McSorley Stephen J
Department of Anatomy, Physiology and Cell Biology, Center for Comparative Medicine, School of Veterinary Medicine, University of California Davis , Davis, CA , USA.
Front Immunol. 2014 Jul 9;5:319. doi: 10.3389/fimmu.2014.00319. eCollection 2014.
Intra-macrophage bacterial infections cause significant morbidity and mortality in both the developed and developing world. Protective host immune responses to these infections initially requires the activation and expansion of pathogen-specific CD4 Th1 cells within lymphoid tissues and subsequent relocation of these effector cells to sites of infection. After entering infected tissues, the elicitation of Th1 bactericidal activity can be triggered by cognate or non-cognate signals that are delivered by locally infected antigen-presenting cells and innate cells. However, the contribution of non-cognate stimulation to the resolution of bacterial infection remains poorly understood, especially in the context of a Th1 response. Here, we review the current data on Th1 cell activation and expansion in mouse models of Salmonella and Chlamydia infection and discuss the potential role of non-cognate Th1 cell stimulation in these disease models. Greater understanding of this pathway of T cell activation may lead to the design of therapeutics or vaccines to combat intra-macrophage pathogens.
巨噬细胞内细菌感染在发达国家和发展中国家都会导致严重的发病和死亡。宿主对这些感染的保护性免疫反应最初需要在淋巴组织内激活和扩增病原体特异性CD4 Th1细胞,并随后将这些效应细胞重新定位到感染部位。进入感染组织后,局部感染的抗原呈递细胞和固有细胞传递的同源或非同源信号可触发Th1杀菌活性。然而,非同源刺激对细菌感染消退的作用仍知之甚少,尤其是在Th1反应的背景下。在此,我们综述了沙门氏菌和衣原体感染小鼠模型中Th1细胞激活和扩增的现有数据,并讨论了非同源Th1细胞刺激在这些疾病模型中的潜在作用。对这一T细胞激活途径的更深入了解可能会导致设计出对抗巨噬细胞内病原体的治疗方法或疫苗。