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  • Title: The truncated MyD88s negatively regulates TLR2 signal on expression of IL17-1 in oyster Crassostrea gigas.
    Author: Fan S, Wang W, Li J, Cao W, Li Q, Wu S, Wang L, Song L.
    Journal: Dev Comp Immunol; 2022 Aug; 133():104446. PubMed ID: 35569578.
    Abstract:
    Toll like receptor (TLR) signaling plays a key role in the innate immune recognition and inflammatory regulation in both vertebrates and invertebrates. The expanded TLR signaling components, including 83 TLRs and 10 MyD88s, have been reported in the genome of the Pacific oyster Crassostrea gigas. In the present study, one endogenous TLR (designated CgTLR2) and two MyD88s (including a full-length CgMyD88-2 containing intact TIR domain and Death-domain, and a truncated CgMyD88s with only TIR domain) were identified from oyster C. gigas. CgTLR2 was highly expressed in haemocytes, especially in granulocytes. The recombinant protein of the extracellular LRR domains of CgTLR2 recognized and bound a variety of PAMPs with the strongest binding capability to LPS. The recombinant protein of intracellular TIR domain of CgTLR2 was able to bind the recombinant proteins of rCgMyD88-2 (KD = 1.96 × 10-9 M) and rCgMyD88s (KD = 4.84 × 10-8 M), with higher affinity towards rCgMyD88-2. After Vibrio splendidus stimulation, the mRNA expression levels of CgTLR2 and CgMyD88-2 were rapidly up-regulated at early stage of immune response (from the 3rd hours after V. splendidus stimulation), while that of CgMyD88s did not change until 24 h post stimulation. When CgTLR2 was knocked-down by siRNA interference, the expression levels of CgMyD88-2 and CgMyD88s decreased significantly, concomitant with the down-regulation of expression of CgIL17-1. After the expression of CgMyD88-2 was interfered, the expressions of CgMyD88s and CgIL17-1 were all decreased. In contrast, after the expression of CgMyD88s was interfered, the expressions of CgMyD88-2 and CgIL17-1 all increased. The results showed that CgMyD88s played a negative role in the regulation of CgTLR2 on inflammatory factor CgIL17-1.
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