查看“抗原提呈”的源代码

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        <strong>抗原提呈</strong>（Antigen Presentation）系适应性免疫应答之始动枢纽，是指专职[[抗原提呈细胞]]（APCs）对内源性或外源性蛋白质进行摄取、有限水解及加工，将其转化为具有免疫活性的“[[抗原肽-MHC复合物]]”（pMHC），呈递于细胞表面供 [[T细胞受体]]（TCR）特异性识别的过程。抗原提呈的保真度与效率不仅决定了[[T细胞]]的激活状态，亦是解构[[肿瘤免疫逃逸]]及制定[[辅助决策]]方案的底层生物学逻辑。
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        <div style="font-size: 1.25em; font-weight: bold; letter-spacing: 1.5px;">抗原提呈 · 数字化图谱</div>
        <div style="font-size: 0.75em; opacity: 0.9; margin-top: 5px; white-space: nowrap;">Antigen Presentation Mechanism (点击展开)</div>
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                [[文件:Antigen_Presentation_Logic.png|220px|抗原加工与提呈路径]]
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            <div style="font-size: 0.85em; color: #475569; margin-top: 15px; font-weight: 600;">内源性与外源性抗原加工路径交互视阈</div>
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                <th style="text-align: left; padding: 12px 18px; border-bottom: 1px solid #f1f5f9; color: #475569; font-weight: 600; width: 35%; background-color: #f8fafc;">关键复合物</th>
                <td style="padding: 12px 18px; border-bottom: 1px solid #f1f5f9; color: #0f172a;">pMHC (肽-MHC)</td>
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                <th style="text-align: left; padding: 12px 18px; border-bottom: 1px solid #f1f5f9; color: #475569; font-weight: 600; background-color: #f8fafc;">核心轴点</th>
                <td style="padding: 12px 18px; border-bottom: 1px solid #f1f5f9; color: #0f172a;">[[交叉提呈]]</td>
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                <th style="text-align: left; padding: 12px 18px; color: #475569; font-weight: 600; background-color: #f8fafc;">临床转化</th>
                <td style="padding: 12px 18px; color: #1e40af; font-weight: bold;">[[新抗原疫苗]]</td>
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<h2 style="background: linear-gradient(to right, #0f172a, #3b82f6); color: #ffffff; padding: 10px 18px; border-radius: 4px; font-size: 1.25em; margin-top: 40px; border-left: 6px solid #1e3a8a;">抗原加工路径的分子动力学</h2>
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    抗原提呈通过高度精密的时空区隔，确保免疫系统对细胞内外蛋白质组的实时监控：
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    <li style="margin-bottom: 15px;"><strong>MHC-I 经典路径：</strong> 胞质内合成的蛋白质（如肿瘤突变蛋白）经[[蛋白酶体]]降解，通过 [[TAP]] 转运蛋白进入内质网，并于[[抗原加工复合物]]中负载至 MHC-I 分子，提呈给 [[CD8+ T细胞]]。该路径之完整性系[[免疫浸润]]型肿瘤之先决条件。</li>
    <li style="margin-bottom: 15px;"><strong>MHC-II 经典路径：</strong> APCs 经由[[胞吞作用]]捕获外源性抗原，在酸性[[内体-溶酶体]]系统中降解并与 MHC-II 分子结合。该过程主导了 [[CD4+ T细胞]] 的募集及[[体液免疫]]的协同。</li>
    <li style="margin-bottom: 15px;"><strong>[[交叉提呈]] (Cross-presentation)：</strong> 树突状细胞（DCs）特有的生物学属性，可将捕获的外源性肿瘤抗原导入 MHC-I 路径。该机制系启动抗肿瘤 [[CTL]] 应答之核心枢纽。</li>
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[Image of cross-presentation in dendritic cells]


<h2 style="background: linear-gradient(to right, #0f172a, #3b82f6); color: #ffffff; padding: 10px 18px; border-radius: 4px; font-size: 1.25em; margin-top: 40px; border-left: 6px solid #1e3a8a;">提呈障碍与肿瘤免疫逃避表型</h2>

<h3 style="color: #1e3a8a; border-bottom: 2px solid #e2e8f0; display: inline-block; padding-bottom: 5px; margin-top: 25px;">1. 抗原提呈链条之分子缄默</h3>
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    肿瘤克隆通过表观遗传及遗传学层面的多重干预，致使提呈效能丧失，诱导形成[[免疫沙漠型]]肿瘤：
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    <li style="margin-bottom: 10px;"><strong>MHC 分子丢失：</strong> 包括 [[B2M]] 基因失活导致的复合物解体及 [[HLA-LOH]]（杂合性丢失）导致的特定新抗原“不可见”。</li>
    <li style="margin-bottom: 10px;"><strong>加工机械缺陷：</strong> 涉及 [[TAP1/2]] 下调或免疫蛋白酶体（LMP2/7）缺陷，致使肽链转运受阻。</li>
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<h3 style="color: #1e3a8a; border-bottom: 2px solid #e2e8f0; display: inline-block; padding-bottom: 5px; margin-top: 25px;">2. 提升提呈效率之干预路径</h3>
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            <th style="padding: 15px; border: 1px solid #cbd5e1; color: #0f172a;">策略维度</th>
            <th style="padding: 15px; border: 1px solid #cbd5e1; color: #0f172a;">分子靶点</th>
            <th style="padding: 15px; border: 1px solid #cbd5e1; color: #0f172a;">临床预期</th>
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            <td style="padding: 12px; border: 1px solid #cbd5e1; font-weight: bold;">表观遗传修饰</td>
            <td style="padding: 12px; border: 1px solid #cbd5e1;">[[HDACi]] / [[DNMTi]]</td>
            <td style="padding: 12px; border: 1px solid #cbd5e1;">恢复 MHC 分子的转录水平</td>
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            <td style="padding: 12px; border: 1px solid #cbd5e1; font-weight: bold;">治疗性疫苗</td>
            <td style="padding: 12px; border: 1px solid #cbd5e1;">[[Neoantigens]] / [[DCs]]</td>
            <td style="padding: 12px; border: 1px solid #cbd5e1;">强制激活原初 T 细胞应答</td>
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    <strong style="color: #1e3a8a; font-size: 1.1em; display: block; margin-bottom: 15px;">参考文献</strong>
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        [1] <strong>Neefjes J, et al. (2011).</strong> <em>Towards a systems understanding of MHC class I and MHC class II antigen presentation.</em> <strong>Nature Reviews Immunology</strong>. <br>
        <span style="color: #1e293b;">[学术点评]：抗原提呈领域的基石文献，完整构建了 MHC 双路径在胞内加工与转运的分子图谱。</span>
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        [2] <strong>Jhunjhunwala S, et al. (2021).</strong> <em>Antigen presentation in cancer: insights into mechanisms and barriers.</em> <strong>Nature Reviews Cancer</strong>. <br>
        <span style="color: #1e293b;">[学术点评]：聚焦于肿瘤微环境对提呈效能的生化抑制，为克服[[间质重塑]]阻碍提供了理论支撑。</span>
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    <p style="margin: 10px 0; border-bottom: 1px solid #e2e8f0; padding-bottom: 10px;">
        [3] <strong>Gettinger S, et al. (2017).</strong> <em>Impaired HLA Class I Antigen Processing and Presentation as a Mechanism of Acquired Resistance to Immune Checkpoint Inhibitors.</em> <strong>Cancer Discovery</strong>. <br>
        <span style="color: #1e293b;">[学术点评]：揭示了抗原加工机械之突变与[[PD-1抑制剂]]获得性耐药间的因果联系。</span>
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    <p style="margin: 10px 0; border-bottom: 1px solid #e2e8f0; padding-bottom: 10px;">
        [4] <strong>Sahin U, et al. (2017).</strong> <em>Personalized RNA mutanome vaccines mobilize poly-specific therapeutic immunity against cancer.</em> <strong>Nature</strong>. <br>
        <span style="color: #1e293b;">[学术点评]：论证了基于个体化提呈肽谱设计新抗原疫苗的可行性及其在引燃免疫应答中的卓越效能。</span>
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        [5] <strong>Embgenbroich M, Burgdorf S. (2018).</strong> <em>Current Concepts of Antigen Cross-Presentation.</em> <strong>Frontiers in Immunology</strong>. <br>
        <span style="color: #1e293b;">[学术点评]：对 DCs 细胞[[交叉提呈]]过程中内体逃逸与肽链负载的动力学特征进行了深度精细解析。</span>
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    <div style="background-color: #0f172a; color: #ffffff; text-align: center; font-weight: bold; padding: 12px; letter-spacing: 2px;">抗原提呈 · 关联导航</div>
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        [[MHC复合物]] • [[树突状细胞]] • [[交叉提呈机制]] • [[新抗原预测]] • [[免疫肽组学]] • [[HLA-LOH]]
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