Why Do We Get Cancer Despite Our Immune Response? Exploring CTLs and Beyond
Why Do We Get Cancer Despite Our Immune Response?
Imagine a robust fortress, equipped with elite soldiers (T-cytotoxic cells or T-CTLs) whose sole mission is to eliminate any potential threat (carcinogenic cells). These soldiers are highly trained and skilled, but sometimes, even the most sophisticated defenses can be breached. In this article, we will explore why T-CTLs might not be enough to prevent cancer and discuss the complex interactions between our immune system and cancer cells.
Understanding the Immune System's Role in Cancer Defense
Cancer is a complex disease that can often bypass the immune system's protective mechanisms. One key player in this battle is T-regulatory cells (Treg cells), which act as a buffer to prevent autoimmune reactions and maintain immune homeostasis. As a result, Treg cells can sometimes inhibit the activity of T-CTLs, making it harder for these warrior cells to do their job effectively.
The term “incipient” refers to the early stages of cancer when tumour cells are just beginning to form. At this stage, the immune system's response can sometimes be insufficient to fully eliminating the cancer. This highlights the importance of understanding the intricate balance between our immune response and cancer progression.
The Role of PD1 and PDL1
Cancer cells are crafty and have developed various strategies to evade detection by the immune system. One common mechanism is the expression of molecules like programmed death 1 (PD1) and programmed death ligand 1 (PDL1). When PD1-PDL1 interactions occur, they can effectively shut down T-CTLs, rendering them ineffective in fighting cancer. These interactions are a primary way that cancer cells can hijack the immune system and promote their own survival.
From the Lab to the Clinic: CTL Cells and Cancer Therapy
Despite the challenges, researchers are actively exploring the use of T-CTLs in cancer treatment. The idea of using a patient's own immune cells (immunotherapy) to target and destroy cancer cells is a promising approach. However, there are several hurdles to overcome:
Immune Suppression from Advanced Cancer: As cancer progresses, it can induce a state of immune suppression in the body. This means that even if T-CTLs are successfully injected, they may not be as effective due to the weakened state of the patient's immune system. Tumour Microenvironment: The area around the tumour (tumour microenvironment) can also be hostile to T-CTLs. Cancer cells secrete chemicals that can inactivate or disable these crucial immune cells, rendering them ineffective. Donor Immune Response: If T-CTLs from another donor are used, they might attack the patient's own cells, leading to complications like graft-versus-host disease (GvHD).While these challenges are real, scientific advancements in areas such as antibody therapy are showing promise. These innovations can enhance the targeting ability and effectiveness of T-CTLs, potentially offering more powerful tools to combat cancer.
Conclusion
In summary, while T-CTLs are an essential part of our immune response to cancer, they are not a panacea. The complex interactions between cancer cells and the immune system highlight the need for a multifaceted approach to cancer treatment. Ongoing research is crucial to developing more effective therapies that can overcome the limitations of current immune-based treatments.
References
David Chan: Link to relevant publication
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