Menon Nivedita, Mariappan Vanitha, Vellasamy Kumutha M, Samudi Chandramathi, See Jia-Xiang, Ganesh P Sankar, Saeidi Alireza, Vadivelu Jamuna, Shankar Esaki Muthu
Department of Medical Microbiology, Faculty of Medicine, University of Malaya, Lembah Pantai, Kuala Lumpur, Malaysia.
Department of Life Sciences, Central University of Tamil Nadu, Thiruvarur 610 005, Tamilnadu, India.
Access Microbiol. 2020 Feb 14;2(5):acmi000110. doi: 10.1099/acmi.0.000110. eCollection 2020.
is the causative agent for melioidosis. Because of its intracellular nature, the bacterium is capable of replicating within a plethora of eukaryotic cell lines. can remain dormant within host cells without symptoms for years, causing recrudescent infections. Here, we investigated the pathogenesis mechanism behind the suppression of T cell responses by . Peripheral blood mononuclear cells (1×10 cells/well) isolated by Ficoll Paque (Sigma-Aldrich) density gradient centrifugation were incubated with optimized concentrations of bacterial crude culture filtrate antigens (CFAs) (10 ug ml) and heat-killed bacteria [1 : 10 multiplicity of infection (m.o.i.)]. Following incubation, cells were investigated for surface expression of coinhibitory molecules by flow cytometry. We found that induced the upregulation of programmed death 1 (PD-1), a molecule responsible for T cell exhaustion, on T cells following exposure to crude CFAs of . This upregulation of PD-1 probably contributes to poor immune surveillance and disease pathogenesis.
是类鼻疽的病原体。由于其细胞内特性,该细菌能够在大量真核细胞系中复制。可在宿主细胞内保持休眠数年而无症状,引发复发感染。在此,我们研究了 抑制T细胞反应背后的发病机制。通过Ficoll Paque(Sigma-Aldrich)密度梯度离心分离的外周血单个核细胞(1×10⁶细胞/孔)与优化浓度的细菌粗培养滤液抗原(CFAs)(10 μg/ml)和热灭活细菌[感染复数(m.o.i.)为1:10]一起孵育。孵育后,通过流式细胞术研究细胞共抑制分子的表面表达。我们发现,在暴露于 的粗CFAs后, 诱导T细胞上程序性死亡1(PD-1)的上调,PD-1是一种导致T细胞耗竭的分子。PD-1的这种上调可能导致免疫监视不良和疾病发病机制。