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上集講述了PD1/PDL1在醫治癌細胞免疫治療方面的重要性，接下來我們將會繼續深入探討問題。257Please respect copyright.ＰＥＮＡＮＡQXjXd53YxG
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上集：https://www.penana.com/article/471125257Please respect copyright.ＰＥＮＡＮＡZpgpbVwnOw
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（圖1）雖然阻擋PD1/PDL1可以增強T cell辨認癌細胞的能力，但另一個重要的問題是，如何確保有足夠的T cell殺滅癌細胞呢?257Please respect copyright.ＰＥＮＡＮＡ6ve0EfPVy4
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就算成功糾正免疫系統細胞懂得把癌細胞辨認為外來之物，但免疫系統細胞數量不足的話，依然是不會達到重大效果的。257Please respect copyright.ＰＥＮＡＮＡbg5Hlu6en3
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換句話說，我們需要一道能夠提升針對癌細胞的T cell數量手段。257Please respect copyright.ＰＥＮＡＮＡNKC3wbO4sJ
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（圖2）T cell的產生數量，接近可以說是由Antigen Presenting Cells(APC)來決定;257Please respect copyright.ＰＥＮＡＮＡLbvMbe5VYa
APC可以睇成為一堆負責把癌細胞獨特Neoantigen帶來T cell面前的細胞。257Please respect copyright.ＰＥＮＡＮＡMFSwo2YBTh
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忘記甚麼是Neoantigen的話，可重溫上一集。257Please respect copyright.ＰＥＮＡＮＡJRcTETlKzs
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當APC展示癌細胞的Neoantigen予T cell的receptor後，另一個必需的動作就是T cell表面的CD28與APC表面的B7合併。257Please respect copyright.ＰＥＮＡＮＡAWsC3vXqBV
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只要兩者條件達成的話，負責對付對應癌細胞的T cell數量及效力便會大增。257Please respect copyright.ＰＥＮＡＮＡnYrkcWvI6Z
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（圖3）然而，當T cell數量產生至一定程度的時候，T cell便會產生出CTLA4。CTLA4會搶奪CD28的位置，與B7合併。257Please respect copyright.ＰＥＮＡＮＡ5EvaXzjPza
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而當CTLA4與B7合併後，T cell所產生的數量及威力就會大減。257Please respect copyright.ＰＥＮＡＮＡr6AZt0kmzc
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這個CTLA4產生的機制是與生俱來的，目的就是為了避免產生過量的T cell，以免身體會產生不良反應。257Please respect copyright.ＰＥＮＡＮＡdP37RpPrtK
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（圖4）只不過的是，現時癌細胞大敵當前，燃眉之急就是要調動大量的T cell前往討伐癌細胞。257Please respect copyright.ＰＥＮＡＮＡeQIlUKORZM
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為此，我們重施應對PD1/PDL1故技，利用抗體阻擋CTLA4，確保CD28及B7持續合併，不斷產生效力高強的T cell。257Please respect copyright.ＰＥＮＡＮＡw0vZFkxxeS
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（圖5）簡略的總結來說，為了確保有足夠的T cell消滅癌細胞，我們不惜採用阻擋CTLA4的抗體，號令身體持續產生效力高強的T cell。257Please respect copyright.ＰＥＮＡＮＡ8HaStNf983
而另一邊廂，我們亦同時利用阻擋PD1/PDL1的抗體，確保T cell能夠順利把癌細胞辨認成為外來物，將其制裁。257Please respect copyright.ＰＥＮＡＮＡ2xthWwgwmf
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這CTLA4抗體及PD1/PDL1抗體的雙管齊下療法，將能大大提升免疫治療的效率。257Please respect copyright.ＰＥＮＡＮＡv7dzNMHAt5
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但是，並不是所有病人也能依靠這方法而得益，原因是T cell沒法能夠順利抵達癌細胞的位置以及滲入癌細胞的內部作有效的消滅。257Please respect copyright.ＰＥＮＡＮＡJS7E9eKPEg
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這一方面，我們將會在下一篇免疫治療的最終章再作探討。257Please respect copyright.ＰＥＮＡＮＡwTUDqf8Zlu
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