查看“TAMs”的源代码

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            <strong>TAMs</strong>（Tumor-Associated Macrophages，肿瘤相关巨噬细胞）是<strong>[[肿瘤微环境]]</strong>（TME）中丰度最高的免疫细胞群体。TAMs 主要由外周血单核细胞募集并分化而来，在肿瘤发展的不同阶段展现出高度的表型可塑性。在<strong>[[促癌炎症]]</strong>的驱动下，TAMs 往往从具有抗肿瘤能力的 <strong>M1型</strong> 向促进肿瘤进展的 <strong>M2型</strong> 极化，通过诱导血管新生、抑制免疫应答及促进<strong>[[组织浸润与转移]]</strong>，成为恶性肿瘤演进的关键“帮凶”。
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            <div style="font-size: 1.2em; font-weight: bold; letter-spacing: 1.2px; text-decoration: none;">TAMs · 生物学概要</div>
            <div style="font-size: 0.75em; opacity: 0.85; margin-top: 4px; white-space: nowrap;">Tumor-Associated Macrophages Profile (点击展开)</div>
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                    [[文件:TAMs_Polarization_Mechanism.png|180px|TAMs 极化机制示意]]
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                <div style="font-size: 0.8em; color: #64748b; margin-top: 12px; font-weight: 500;">图：TAMs 从 M1 向 M2 型的转化路径</div>
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                    <th style="text-align: left; padding: 10px 15px; border-bottom: 1px solid #f1f5f9; color: #475569; background-color: #f8fafc; width: 40%;">通用标志物</th>
                    <td style="padding: 10px 15px; border-bottom: 1px solid #f1f5f9; color: #0f172a;"><strong>CD68</strong>, <strong>F4/80</strong></td>
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                    <th style="text-align: left; padding: 10px 15px; border-bottom: 1px solid #f1f5f9; color: #475569; background-color: #f8fafc;">M2型标志物</th>
                    <td style="padding: 10px 15px; border-bottom: 1px solid #f1f5f9; color: #0f172a;"><strong>CD163</strong>, <strong>CD206</strong>, <strong>Arg-1</strong></td>
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                    <th style="text-align: left; padding: 10px 15px; color: #475569; background-color: #f8fafc;">关键转录因子</th>
                    <td style="padding: 10px 15px; color: #1e40af; font-weight: 600;"><strong>STAT3</strong>, <strong>IRF4</strong></td>
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        TAMs 的生物学功能高度依赖于其在微环境信号驱动下的表型极化：
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        <li style="margin-bottom: 12px;"><strong>免疫极化转换：</strong> 在肿瘤分泌的 <strong>IL-10</strong>、<strong>TGF-β</strong> 及 <strong>CSF-1</strong> 作用下，TAMs 表现为 <strong>M2型</strong> 表型，丧失抗原提呈能力。</li>
        <li style="margin-bottom: 12px;"><strong>血管新生驱动：</strong> TAMs 是微环境中 <strong>VEGF</strong> 和 <strong>PIGF</strong> 的主要来源，通过“血管模拟”促进肿瘤内部血氧供应。</li>
        <li style="margin-bottom: 12px;"><strong>免疫抑制构建：</strong> 通过表达 <strong>PD-L1</strong> 和释放外泌体，TAMs 能直接诱导效应 <strong>CD8+ T细胞</strong> 耗竭，屏蔽 <strong>NK细胞</strong> 的杀伤活性。</li>
        <li style="margin-bottom: 12px;"><strong>基质重塑与转移：</strong> 分泌基质金属蛋白酶（<strong>MMPs</strong>），降解细胞外基质，为肿瘤细胞的远端迁徙开辟路径。</li>
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    <h2 style="background: #f1f5f9; color: #0f172a; padding: 10px 18px; border-radius: 0 6px 6px 0; font-size: 1.25em; margin-top: 40px; border-left: 6px solid #0f172a; font-weight: bold; text-decoration: none;">M1型 vs. M2型巨噬细胞对比表</h2>

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                <th style="padding: 12px; border: 1px solid #cbd5e1; color: #0f172a; width: 25%;">特征维度</th>
                <th style="padding: 12px; border: 1px solid #cbd5e1; color: #1e40af;">M1型 (典型活化)</th>
                <th style="padding: 12px; border: 1px solid #cbd5e1; color: #dc2626;">M2型 (替代活化/TAMs)</th>
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                <td style="padding: 10px; border: 1px solid #cbd5e1; font-weight: 600;">诱导因素</td>
                <td style="padding: 10px; border: 1px solid #cbd5e1;">IFN-γ, LPS</td>
                <td style="padding: 10px; border: 1px solid #cbd5e1;">IL-4, IL-13, TGF-β</td>
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                <td style="padding: 10px; border: 1px solid #cbd5e1; font-weight: 600;">主要功能</td>
                <td style="padding: 10px; border: 1px solid #cbd5e1;">促炎、吞噬病原体、抗肿瘤</td>
                <td style="padding: 10px; border: 1px solid #cbd5e1;">抑炎、组织修复、促血管新生</td>
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                <td style="padding: 10px; border: 1px solid #cbd5e1; font-weight: 600;">代谢特征</td>
                <td style="padding: 10px; border: 1px solid #cbd5e1;"><strong>糖酵解</strong> 增强 (类似 Warburg)</td>
                <td style="padding: 10px; border: 1px solid #cbd5e1;"><strong>脂肪酸氧化</strong> (FAO) 与 <strong>OXPHOS</strong></td>
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        <span style="color: #0f172a; font-weight: bold; font-size: 1.05em; display: inline-block; margin-bottom: 5px;">参考文献与学术点评</span>
        
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            [1] <strong>Mantovani A, et al. (2002).</strong> <em>Macrophage plasticity and polarization in cancer.</em> <strong>Trends in Immunology</strong>. <br>
            <span style="color: #475569;">[学术点评]：该研究奠定了巨噬细胞在肿瘤微环境中的极化理论，明确了 M1/M2 二元分类的基本框架。</span>
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            [2] <strong>Noy R, Pollard J W. (2014).</strong> <em>Tumor-associated macrophages: from mechanisms to therapy.</em> <strong>Immunity</strong>. <br>
            <span style="color: #475569;">[学术点评]：系统综述了 TAMs 在肿瘤进展中的多重角色，并提出了针对 TAMs 募集与重编程的治疗策略。</span>
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            [3] <strong>Cassetta L, Pollard J W. (2018).</strong> <em>Targeting macrophages: therapeutic approaches in cancer.</em> <strong>Nature Reviews Drug Discovery</strong>. <br>
            <span style="color: #475569;">[学术点评]：权威分析了当前临床上靶向 TAMs 的各种途径，包括阻断 CSF-1R 信号通路等前沿进展。</span>
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        <div style="background-color: #0f172a; color: #ffffff; text-align: center; font-weight: bold; padding: 10px; letter-spacing: 1px;">TAMs · 知识图谱关联</div>
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            [[肿瘤微环境]] • [[促癌炎症]] • [[免疫逃逸]] • [[M1/M2极化]] • [[MSC-TAM互作]] • [[外泌体通讯]]
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