Some research advances of immune mechanism during infection in China

Yang, Wei

Although these responses are physiologically designed for the defense against pathogens, their inappropriate or poorly restricted activation drives inflammatory disorders and causes host pathology. Thus, not only pathogen-associated molecular pattern recognition but also inflammatory process are normally under stringent regulation. A novel pathway mediated by CD24 and its receptor is essential in self-nonself discrimination in pattern recognition, enabling to initiate immunity against pathogens without significant immune-mediated self-destruction in case of tissue injuries [25] . Recent studies have revealed that conventional T cells dampen the innate immune response during the early phases of infection, and effector and memory T cells dampen the hyperactive inflammasome during late phase of primary responses or on secondary challenges, regulating host immunity appropriately [26] . In addition, regulators, such as soluble TLRs, growth arrest-specific gene 6 (Gas6), suppressor of tumorigenicity (ST2) and so on, act at multiple levels within TLR signaling transduction [27, 28] . As a transcriptional factor significantly involved in inflammation, Kruppel-like factor 4 (KLF4) inhibits LPS-induced IL-6 release and thus limits potentially harmful immunopathological consequences [29] . Some mechanisms are employed by negative regulators to ensure the appropriate modulation of immune response [30] [31] [32] .