Self-assembled peptide nanofibers raise significant antibody and T cell responses without adjuvants, but the mechanism by which they achieve this has not been fully elucidated. Myeloid differentiation primary response gene 88 (MyD88) has previously been shown to be critical for the antibody response to antigens presented by peptide nanofibers. The present study sought to determine the cell subset in which MyD88 is essential for T cell responses. Mice deficient in MyD88 or CD11c⁺ cells had severely attenuated T cell responses. However, mice lacking MyD88 in only CD11c⁺ cells remained capable of internalizing, processing, and presenting nanofiber-derived epitopes to stimulate T cell responses. The necessity of the inflammasome pathway was ruled out. Using adoptive transfer models where MyD88 was eliminated in CD4⁺ T cells or in the host, we observed that deficiency only in T cells or only in the host had no impact on the T cell response to nanofiber vaccines. Therefore, knocking out MyD88 in either antigen-presenting cells (APCs) or CD4 T cells could not compromise the CD4 T cell responses, suggesting that self-assembled peptide nanofibers trigger redundant MyD88-dependent and MyD88-independent signaling pathways in APCs and T cells. Similar redundancy has been observed for other adjuvants, and this is discussed.

中文翻译：

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肽纳米纤维疫苗接种期间 ，抗原呈递细胞中的MyD88不需要CD4 ⁺ T细胞应答†

自组装的肽纳米纤维在没有佐剂的情况下会产生显着的抗体和T细胞应答，但尚未完全阐明其实现这种作用的机制。先前已经证明了髓样分化初级应答基因88（MyD88）对于肽纳米纤维对抗原的抗体应答至关重要。本研究试图确定其中MyD88对于T细胞反应至关重要的细胞亚群。MyD88或CD11c ⁺细胞不足的小鼠的T细胞反应严重减弱。但是，仅CD11c ^+中缺少MyD88的小鼠细胞仍然能够内在化，加工并呈递纳米纤维衍生的表位来刺激T细胞反应。排除了炎性体途径的必要性。使用过继转移模型，其中MyD88在CD4 ⁺ T细胞或宿主中被消除，我们观察到仅T细胞或宿主中的缺乏对T细胞对纳米纤维疫苗的反应没有影响。因此，敲除抗原呈递细胞（APC）或CD4 T细胞中的MyD88不会损害CD4 T细胞的反应，这表明自组装肽纳米纤维在APC和T细胞中触发了冗余的MyD88依赖性和MyD88依赖性信号通路。对于其他佐剂也观察到了类似的冗余，对此进行了讨论。