Your Immune System

You're told your immune system fights infection. What you're rarely told is that it's also your primary defense against cancer — and that defense may be compromised long before you're diagnosed.

Every day, your body produces cells that could become cancerous. A functioning immune system finds and destroys them. This isn't alternative medicine — it's basic immunology. The reason you don't have cancer most of the time is because your immune system is doing its job.

When that system fails — through chronic stress, poor sleep, environmental toxins, or the cancer itself — malignant cells slip through. And once cancer establishes itself, it actively suppresses the immune response to protect itself.

Understanding this changes everything. Treatment isn't just about killing cancer cells. It's about restoring the system that should have caught them in the first place.

Your immune system has two main branches:

Innate immunity — the first responders. Fast, non-specific, always on patrol. This includes Natural Killer (NK) cells.

Adaptive immunity — the specialists. Slower to activate, but highly targeted. This includes T cells and B cells.

Both matter for cancer. Here's how they work:

Natural Killer (NK) Cells

NK cells are your body's first-line cancer surveillance. They don't need to be trained — they recognize abnormal cells on contact and kill them immediately.

Research shows:

• People with lower NK cell activity have higher cancer incidence
• People with higher NK cell activity have better outcomes after diagnosis
• NK cell function declines with age, chronic stress, and poor sleep

NK cells are why most mutated cells never become tumors. They're killed before they can establish themselves. When NK function drops, the probability of a cancer cell surviving goes up.

What suppresses NK cells:

• Chronic psychological stress (elevated cortisol)
• Sleep deprivation (even one night reduces NK activity by 70%)
• Chronic inflammation
• Certain chemotherapy drugs
• The tumor itself (cancer cells secrete compounds that suppress NK function)

T Cells

T cells are the adaptive immune system's cancer killers. Unlike NK cells, they need to be activated and trained to recognize specific threats.

CD8+ Cytotoxic T cells — directly kill cancer cells they've been trained to recognize

CD4+ Helper T cells — coordinate the immune response, activate other immune cells

Regulatory T cells (Tregs) — suppress immune activity to prevent autoimmunity. Cancer can hijack these to protect itself.

T cells are what checkpoint inhibitors target.

The Checkpoint System

Your immune system has built-in brakes — "checkpoints" that prevent it from attacking healthy tissue. Cancer cells exploit these brakes to hide.

The two main checkpoints:

PD-1/PD-L1 — T cells have PD-1 receptors. When they bind to PD-L1 (found on some cells), the T cell stands down. Many cancers express PD-L1 specifically to trigger this "don't attack" signal.

CTLA-4 — another brake that prevents T cell activation.

Checkpoint inhibitors (Opdivo, Keytruda, Yervoy) release these brakes. They block PD-1, PD-L1, or CTLA-4, allowing T cells to attack the cancer.

This is why immunotherapy works differently than chemo. Chemo poisons fast-dividing cells. Immunotherapy unleashes your own immune system.

T Cell Exhaustion

Here's what most patients aren't told: chronic activation wears T cells out.

When T cells are constantly stimulated — by a persistent infection or an ongoing cancer — they enter a state called "exhaustion." This isn't just fatigue. It's a measurable cellular state:

• Reduced ability to kill target cells
• Reduced cytokine production
• Altered gene expression
• Potentially irreversible changes

The stages:

Early exhaustion — T cells still function but at reduced capacity. Largely reversible.

Terminal exhaustion — T cells are functionally depleted. May be permanent.

Epigenetic lock-in — Research suggests that beyond a certain point, the changes become irreversible at the DNA level.

This matters because checkpoint inhibitors work by keeping T cells activated. Long-term treatment may push T cells from early exhaustion into terminal exhaustion.

The question nobody has funding to answer: at what point does continued treatment cause more immune damage than benefit?

What Checkpoint Inhibitors Actually Do

They release the brakes on your T cells. That's it. They don't create new immune cells. They don't repair exhausted ones. They just remove the "off switch" that cancer was using.

For patients who respond, this can be transformative. T cells that were being suppressed suddenly attack the tumor.

But there's a cost:

• The same brakes that cancer exploits also prevent autoimmunity
• Removing them can cause immune-related adverse events (colitis, hepatitis, thyroiditis, etc.)
• Chronic activation may accelerate T cell exhaustion

The immunotherapy business model keeps patients on treatment indefinitely. The biology suggests this may not be optimal for long-term immune health.