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논문 기본 정보

자료유형
학술저널
저자정보
Jae-Hyung Lee (Chungnam National University College of Medicine) Jae-Min Yuk (Chungnam National University College of Medicine) Guang-Ho Cha (Chungnam National University College of Medicine) Young-Ha Lee (Chungnam National University College of Medicine)
저널정보
대한기생충학열대의학회 Parasites, Hosts and Diseases Parasites, Hosts and Diseases Vol.61 No.2
발행연도
2023.5
수록면
138 - 147 (10page)

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Toxoplasma gondii is an intracellular protozoan parasite which can infect most warmblooded animals and humans. Among the different mouse models, C57BL/6 mice are more susceptible to T. gondii infection compared to BALB/c mice, and this increased susceptibility has been attributed to various factors, including T-cell responses. Dendritic cells (DCs) are the most prominent type of antigen-presenting cells and regulate the host immune response, including the response of T-cells. However, differences in the DC responses of these mouse strains to T. gondii infection have yet to be characterized. In this study, we cultured bone marrow-derived DCs (BMDCs) from BALB/c and C57BL/6 mice. These cells were infected with T. gondii. The activation of the BMDCs was assessed based on the expression of cell surface markers and cytokines. In the BMDCs of both mouse strains, we detected significant increases in the expression of cell surface Tcell co-stimulatory molecules (major histocompatibility complex (MHC) II, CD40, CD80, and CD86) and cytokines (tumor necrosis factor (TNF)-α, interferon (IFN)-γ, interleukin (IL)-12p40, IL-1β, and IL-10) from 3 h post-T. gondii infection. The expression of MHC II, CD40, CD80, CD86, IFN-γ, IL-12p40, and IL-1β was significantly higher in the T. gondiiinfected BMDCs obtained from the C57BL/6 mice than in those from the BALB/c mice. These findings indicate that differences in the activation status of the BMDCs in the BALB/c and C57BL/6 mice may account for their differential susceptibility to T. gondii.

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Abstract
Introduction
Materials and Methods
Results
Discussion
References

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UCI(KEPA) : I410-ECN-0101-2023-513-001473081