CpG oligodeoxynucleotides enhance FcγRI-mediated cross presentation by dendritic cells
CpG oligodeoxynucleotides enhance FcγRI-mediated cross presentation by dendritic cells
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DOI：
10.1093/intimm/dxh110
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发表时间：
2004-08-01
影响因子：
4.4
通讯作者：
Van Vugt, MJ
中科院分区：
文献类型：
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作者：
Bevaart, L;Van Ojik, HH;Van Vugt, MJ
树突状细胞（DC）可以通过其通过主要组织相容性复合体I类途径交叉呈递外源抗原的能力触发幼稚CD8(+) T细胞反应。骨髓I类IgG受体FcgammaRI （CD64）在DC上表达，在体内将抗原靶向FcgammaRI可诱导强烈的体液和细胞免疫反应。我们研究了人FcgammaRI （hFcgammaRI）促进dc介导的交叉呈递和T细胞活化的能力，并评估了CpG寡脱氧核苷酸对这一过程的影响。我们从hFcgammaRI转基因小鼠中获得表达未成熟DC的hFcgammaRI，从非转基因小鼠获得表达未成熟DC的hFcgammaRI。抗原作为卵清蛋白免疫复合物靶向Fcgamma受体，或通过卵清蛋白- cd64 mAb融合蛋白选择性靶向hFcgammaRI。未成熟DC与CpG ODN共孵育可显著增加fcgammar靶向抗原的MHC I类呈递。当OVA选择性靶向hFcgammaRI时，Tg和NTg DC之间几乎没有差异。然而，与CpG ODN共孵育后，hfcgammari触发的交叉呈现增强。这些结果证明了hFcgammaRI在DC上与CpG ODN共培养后通过MHC I类触发交叉呈现的能力。
Dendritic cells (DC) can trigger naive CD8(+) T cell responses by their capacity to cross-present exogenous antigens via the major histocompatibility complex class I pathway. The myeloid class I IgG receptor, FcgammaRI (CD64), is expressed on DC, and in vivo targeting of antigens to FcgammaRI induces strong humoral and cellular immune responses. We studied the capacity of human FcgammaRI (hFcgammaRI) to facilitate DC-mediated cross presentation and T cell activation, and assessed the effect of CpG oligodeoxynucleotides on this process. We generated hFcgammaRI expressing immature DC from hFcgammaRI transgenic and immature DC from non-transgenic mice. Antigens were targeted to Fcgamma receptors as ovalbumin immune complexes, or selectively to hFcgammaRI via ovalbumin-CD64 mAb fusion proteins. Co-incubation of immature DC with CpG ODN led to markedly increased MHC class I presentation of FcgammaR-targeted antigens. When OVA was selectively targeted to hFcgammaRI, few differences were observed between Tg and NTg DC. However, upon co-incubation with CpG ODN, hFcgammaRI-triggered cross presentation was enhanced. These results document the capacity of hFcgammaRI on DC to trigger cross presentation via MHC class I upon co-culture with CpG ODN.