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圖解:PD-L1的表達影響A型流感感染過程

2013年04月09日 07:39:44人氣:1070來源:上海士鋒生物科技有限公司

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關(guān) 鍵 詞細胞,抗體
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有證據(jù)表明不變的自然殺傷T(iNKT)細胞在防護對抗A型流感病毒中發(fā)揮重要的作用。然而,抑制受體,程序性死亡因子1(PD1)及其配體,程序性死亡配體(PK-L)1和2在iNKT細胞上防護對抗A型流感病毒中的作用被證實。研究人員調(diào)查了在iNKT細胞上的這些共刺激分子的對流行性感冒的效應(yīng)。

Figure 1 iNKT cells reduce the sensitivity of BALB/c mice to IAV infection.

文中研究結(jié)果證明iNKT細胞減少了對IAV的敏感性導(dǎo)致PK-L1表達的缺乏,并且在IAV后PD-L2是抑制有害炎癥應(yīng)答中PD-L2的存在具有重要作用。

原文摘要:

Lack of PD-L1 Expression by iNKT Cells Improves the Course of Influenza A Infection

Hadi Maazi,Abinav K. Singh,Anneliese O. Speak,Vincent Lombardi,Jonathan Lam,Bryant Khoo,Kyung Soo Inn,Arlene H. Sharpe,Jae U. Jung,Omid Akbari

There is evidence indicating that invariant Natural Killer T (iNKT) cells play an important role in defense against influenza A virus (IAV). However, the effect of inhibitory receptor, programmed death-1 (PD-1), and its ligands, programmed death ligand (PD-L) 1 and 2 on iNKT cells in protection against IAV remains to be elucidated. Here we investigated the effects of these co-stimulatory molecules on iNKT cells in the response to influenza. We discovered that compare to the wild type, PD-L1 deficient mice show reduced sensitivity to IAV infection as evident by reduced weight loss, decreased pulmonary inflammation and cellular infiltration. In contrast, PD-L2 deficient mice showed augmented weight loss, pulmonary inflammation and cellular infiltration compare to the wild type mice after influenza infection. Adoptive transfer of iNKT cells from wild type, PD-L1 or PD-L2 deficient mice into iNKT cell deficient mice recapitulated these findings. Interestingly, in our transfer system PD-L1−/−-derived iNKT cells produced high levels of interferon-gamma whereas PD-L2−/−-derived iNKT cells produced high amounts of interleukin-4 and 13 suggesting a role for these cytokines in sensitivity to influenza. We identified that PD-L1 negatively regulates the frequency of iNKT cell subsets in the lungs of IAV infected mice. Altogether, these results demonstrate that lack of PD-L1 expression by iNKT cells reduces the sensitivity to IAV and that the presence of PD-L2 is important for dampening the deleterious inflammatory responses after IAV infection. Our findings potentially have clinical implications for developing new therapies for influenza.

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