作者: Jin Li , Lili Zhang , Xin Chen , Ding Chen , Xia Hua
DOI: 10.1038/SREP36150
关键词: Innate immune system 、 Conjunctiva 、 NFKB1 、 Immunity 、 Interleukin-1 Receptor-Like 1 Protein 、 TLR4 、 Immunology 、 Interleukin 33 、 Allergic inflammation 、 Biology
摘要: Innate immunity has been extended to respond environmental pathogen other than microbial components. Here we explore a novel pollen/TLR4 innate in allergic inflammation. In experimental conjunctivitis induced by short ragweed (SRW) pollen, typical signs, stimulated IL-33/ST2 signaling and overproduced Th2 cytokine were observed ocular surface, cervical lymph nodes isolated CD4+ T cells of BALB/c mice. These clinical, cellular molecular changes significantly reduced/eliminated TLR4 deficient (Tlr4-d) or MyD88 knockout (MyD88−/−) Aqueous SRW extract (SRWe) directly IL-33 mRNA protein expression corneal epithelium conjunctiva wild type, but not Tlr4-d MyD88−/− mice with topical challenge. Furthermore, SRWe-stimulated production was blocked antibody NF-kB inhibitor mouse human epithelial cells. findings for the first time uncovered mechanism which pollen initiates TLR4-dependent that triggers Th2-dominant