Immunome Research
Open Access
ISSN: 1745-7580
ISSN: 1745-7580
Seong Kug Eo, Junu Aleyas George, Seong Bum Kim, Jin Young Choi, Ajit Mahadev Patil, Ferdaus Mohd Altaf Hossain and Erdenebelig Uyangaa
Chonbuk National University, Republic of South Korea
Posters & Accepted Abstracts: Immunome Res
Possible risk mediators in primary dengue virus (DenV) infection that favor secondary DenV infection to life-threatening dengue hemorrhagic fever (DHF) and shock syndrome (DSS) via antibody-dependent enhancement (ADE) have not yet been described. Here, DenV infection enhanced the expression of inflammatory mediators and activation molecules in dendritic cells (DCs) through TLR2/MyD88 pathway. TLR2 appeared to facilitate DenV infection in DCs that were less permissive than macrophages for viral replication. In experiments using separate evaluations of DenV-infected and uninfected bystander DCs, infected DCs showed impaired maturation accompanied with TLR2-dependent production of inflammatory cytokines, by which uninfected bystander DCs showed increased expression of co-stimulatory molecules. Differential phosphorylation of MAPK and STAT3 was also detected between DenV-infected and uninfected DCs. Furthermore, DenV infection stimulated Th2-polarized humoral and cellular immunity against foreign and DenV Ag via TLR2/MyD88 pathway, and DenV-infected DCs were revealed to facilitate Th2-biased immune responses in TLR2-dependent manner. TLR2/MyD88-mediated Th2biased Ab responses to primary DenV infection increased the infectivity of secondary homotypic or heterotypic DenV via ADE. Collectively, these results indicate that TLR2/MyD88 pathway in DC-priming receptors can drive Th2-biased immune responses during primary DenV infection, which could favor secondary DenV infection to DHF/DSS via ADE. Recent Publications 1. Katzelnick L C, Coloma J, Harris E (2017) Dengue: Knowledge gaps, unmet needs, and research priorities. The Lancet Infect. Dis. 17(3): e88-e100. 2. Modhiran N, Watterson D, Muller D A, Panetta A K, Sester D P et al. (2015) Dengue virus NS1 protein activates cells via Toll-like receptor 4 and disrupts endothelial cell monolayer integrity. Sci. Transl. Med. 7: 304ra142. 3. Chen J, Ng M M, Chu J J (2015) Activation of TLR2 and TLR6 by dengue NS1 protein and its implications in the immunopathogenesis of dengue virus infection. PLoS Pathog. 11(7): e1005053.
Seong Kug Eo in his lab, has focused on unveiling how hosts response to pathogen infection. They have used various infectious models to prove host responses upon pathogenic infection. His lab has recently found the detailed pathway that IFN-I signal pathway orchestrated environments to provide effective protection against mucosal viral infection. Moreover, his lab is expert on viral acute encephalitis caused by flavivirus infection.
Email:vetvirus@chonbuk.ac.kr