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。1586Please respect copyright.ＰＥＮＡＮＡ5i5LWpayub
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上集：https://www.penana.com/article/4711251586Please respect copyright.ＰＥＮＡＮＡY5bRh6sPv4
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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?1586Please respect copyright.ＰＥＮＡＮＡaQzYUFITOh
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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。1586Please respect copyright.ＰＥＮＡＮＡIlftiYSz52
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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。1586Please respect copyright.ＰＥＮＡＮＡLOVA7CVz1K
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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;1586Please respect copyright.ＰＥＮＡＮＡxyOOxevpF4
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。1586Please respect copyright.ＰＥＮＡＮＡvoayXCrHgC
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忘記甚麼是Neoantigen的話，可重溫上一集。1586Please respect copyright.ＰＥＮＡＮＡrqWTNiQsnO
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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。1586Please respect copyright.ＰＥＮＡＮＡbBbYtb7mPW
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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。1586Please respect copyright.ＰＥＮＡＮＡU2J4NwRTWx
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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。1586Please respect copyright.ＰＥＮＡＮＡ4ORMRn7VRi
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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。1586Please respect copyright.ＰＥＮＡＮＡGrkLNsWeO8
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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。1586Please respect copyright.ＰＥＮＡＮＡWiygEtQpzu
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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。1586Please respect copyright.ＰＥＮＡＮＡw9EcjATvVq
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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。1586Please respect copyright.ＰＥＮＡＮＡDvxn5Q0TRG
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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。1586Please respect copyright.ＰＥＮＡＮＡD8OvaSgNWI
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。1586Please respect copyright.ＰＥＮＡＮＡmI0Vf80ikZ
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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。1586Please respect copyright.ＰＥＮＡＮＡs4Qn9MrDNN
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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。1586Please respect copyright.ＰＥＮＡＮＡAdVqXO0HN8
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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。1586Please respect copyright.ＰＥＮＡＮＡCxkWPB3rIU
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如果想我快啲出文的話，請入去Penana網站科普專欄–薯不揀單俾一個like以及Bookmark，這對我非常之重要。1586Please respect copyright.ＰＥＮＡＮＡRgw9bOyVf2
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