Toll-like receptors, an important family of the PRRs which are well characterized in vertebrates, initiate a signaling cascade which leads to activation of the Myeloid differentiation factor 88 and the transcription factor nuclear factorkappaB. MyD88 consists of a Toll/interleukin-1 receptor domain and a death domain and is the common signaling adaptor protein shared by all TLRs except TLR3. The TIR domain is essential to the interactions between TLRs and MyD88. The death domain, in turn, associates with the death domain of interleukin-1 receptor associated kinase, to trigger downstream signaling cascades that lead to the activation of the NF-kB. MyD88 was first identified in 1990 and has been extensively studied in many species, including human, porcine, mouse, chicken, reptiles, fish, scallop and flies. To date, variants of MyD88 have been reported only in several vertebrates such as humans, mice and chicken. Recent studies have shown that MyD88 genes are duplicated in common carp. Although the MyD88 gene has been sequenced in diplostraca and anostraca little is known about its extence in in penaeidae. The Pacific white shrimp, Litopenaeus vannamei, is distributed along the Pacific coast ranging from the Gulf of California to the northern Peru and has become one of the most important economic penaeid shrimps worldwide, particularly in the Eastern Pacific region and Asia. With rapid expansion of farming, bacterial and viral diseases have become a major concern, causing substantial economic losses in many countries since the 1990s. For example, the white spot syndrome virus is one of the most common and destructive pathogen and is able to cause 100% mortality within 3 days to 10 days after infection. Study on the L. vannamei CHIR-99021 immune system is much needed in order to design better strategies for disease prevention and control. Our previous studies suggest that a signaling cascade similar to the TLR/MyD88/Tube/Pelle/TRAF6/NF-kB pathway may exist in L. vannamei, and could be activated by wsv449, to upregulate the expression of wsv069, wsv303, and wsv371. Several key genes in this pathway, including the Toll genes, the Pelle gene, the TRAF6 gene, and the Rel/NF-kB homologous genes, have been characterized. In this study, two variants of the MyD88 gene were identified in L. vannamei and their function was studied in signal transduction in response to different stimuli. To better understand the roles of LvMyD88 in response to exposure to various potential pathogens in L. vannamei, the expression of LvMyD88 was investigated in hemocytes after stimulation with the ligands of different TLRs, gram-negative bacterium V. parahaemolyticus, gram-positive bacterium S. aureus and viral pathogen WSSV. After poly I:C stimulation, the transcriptional level of the LvMyD88 was lower than that of the control group at all time points except 4 h and 12 h. LvMyD88 was upregulated after stimulation with LPS and CpG-ODN2006, V. parahaemolyticus, S. aureus and WSSV. Particularly, LvMyD88 were strongly upregulated after LPS and S. aureus challenged. Probably due to the differences in the TLRs involved in recognizing the different PAMPs involved in each stimulation experiment. All the results suggested that LvMyD88 may play a role in innate immune in L. vannamei. In Drosophila, it is known that the Toll pathway is central to host anti-bacterial and anti-viral response by regulating the expression of the immune related genes, including AMPs.