Szabo Peter A, Goswami Ankur, Memarnejadian Arash, Mallett Christiane L, Foster Paula J, McCormick John K, Haeryfar S M Mansour
Department of Microbiology and Immunology.
Department of Medical Biophysics Robarts Research Institute.
J Infect Dis. 2016 Jun 15;213(12):1990-5. doi: 10.1093/infdis/jiw050. Epub 2016 Feb 9.
Toxic shock syndrome (TSS) and other superantigen-mediated illnesses are associated with 'systemic' immunosuppression that jeopardizes the host's ability to fight pathogens. Here, we define a novel mechanism of 'local' immunosuppression that may benefit the host. Systemic exposure to staphylococcal enterotoxin B (SEB) rapidly and selectively recruited CD11b(+)Gr-1(high)Ly-6C(+) granulocytic myeloid-derived suppressor cells (MDSCs) to the liver of HLA-DR4 transgenic mice. Hepatic MDSCs inhibited SEB-triggered T cell proliferation in a reactive oxygen species-dependent manner, and ex vivo-generated human MDSCs also similarly attenuated the proliferative response of autologous T cells to SEB. We propose a role for MDSCs in mitigating excessive tissue injury during TSS.
中毒性休克综合征（TSS）及其他超抗原介导的疾病与“全身性”免疫抑制相关，这种免疫抑制会损害宿主对抗病原体的能力。在此，我们定义了一种可能对宿主有益的“局部”免疫抑制新机制。全身性暴露于葡萄球菌肠毒素B（SEB）会迅速且选择性地将CD11b(+)Gr-1(高)Ly-6C(+)粒细胞性骨髓来源的抑制细胞（MDSCs）募集至HLA-DR4转基因小鼠的肝脏。肝脏MDSCs以依赖活性氧的方式抑制SEB触发的T细胞增殖，并且体外生成的人MDSCs同样也能减弱自体T细胞对SEB的增殖反应。我们提出MDSCs在减轻TSS期间过度的组织损伤中发挥作用。
