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Updated August 05, 2015.

Introduction

Cancer cells often have a number of changes in their genes that make them very adaptable. Sometimes the battle needs to be fought on a number of different fronts simultaneously.

One such front involves the Cancer-Immunity Cycle -- a series of steps that can influence whether the immune response to the cancer is weak, like a pebble hitting a truck, or strong, like an all-out assault that's effective at killing the cancer cells.

The Cancer-Immunity Cycle

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Overview

• As cancer cells die, they release antigens, or substances that can be recognized by the immune system.
• Antigens from the cancer cells are then taken up and presented on the cell surface of special immune cells so that other immune cells can “see” the antigens of interest.
• This leads to the activation of T cells, which then travel via the blood vessels to reach the tumor, infiltrate it, recognize the cancer cells and kill them.

Step 1

Mutations in cancer cells cause the release of substances called “antigens” that show that cancer cells are different from normal cells. This allows the immune system to recognize them.

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More on Step 1:

As you know, your immune system has the ability to recognize foreign invaders like bacteria and viruses. But did you know your immune system also detects what might be described as “shoddy or foreign construction?” That’s right – a veritable chunk of bricks and mortar that your body assesses and quickly deems “not my product, not of my construction, therefore foreign.”

Chunks may be bits of the cell wall from a dead bacterium, a piece of protein from a virus, or part of a capsule formed by bacteria, for instance; but foreign materials may also arise from within, as they do in cancer.

Cancer cells accumulate a number of genetic changes. Changes may result in differences from self -- that is, detectible differences on the cancer cells that the immune system can latch onto.

These parts of cancer cells that the immune system can recognize as foreign are called “neoantigens.” They arise from our own cells, gone amuck with caner -- rather than, say, an invading influenza virus, which has plenty of antigens.

Step 2

Immune cells that specialize in finding antigens capture the released antigens and take them to T cells, located in the lymph nodes. Immunotherapy can boost immunity at this step and others.

Step 3

T cells become ‘primed’ or ‘activated’ by these foreign antigens, which begins the immune response against cancer cells.

Step 4

Activated T cells travel through blood vessels towards the location of the tumor.

Step 5

T cells reach the cancer cells and “infiltrate” the tumor in order to attack it.

Step 6

T cells are able to recognize foreign cancer cells based on the antigens they released earlier.

Step 7

T cells destroy cancer cells by activating a series of steps that lead to cell death. This another step at which immunotherapy can help enhance immunity.

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More on Step 7:

T cells, members of the immune system’s “army,” may be able to recognize neoantigens from cancer cells, but a powerful attack by T cells on the malignant cells is still far from guaranteed. Sometimes the cells in the area of the tumor result in a dialing down the T-cell response to the cancer.

You know those dimmer switches that let you set the mood lighting in dining rooms and such? Well, that dimmer switch is technically a kind of rheostat, or a device that lets you vary the resistance in an electrical circuit without interrupting the circuit.

Sometimes there is a dimmer switch of sorts that diminishes the immune system’s anti-cancer efforts. The dimmer switch operates in the place where tumors grow and interact with other cells -- the tumor microenvironment. According to a July 2013 article published in “Immunity,” factors in the tumor microenvironment can act to restrain activated antitumor T cell immune responses, acting as an immune rheostat or ‘‘immunostat.’’

The immune rheostat is not completely understood, however certain molecules that are important in how the immune system interacts with cancer have been identified, including programmed death-ligand 1, or PD-L1, and programmed death-1, or PD-1.

Agents that inhibit the inhibition from this dimmer switch represent one way of preventing cancer from disabling T cells in the tumor microenvironment.

Sources and Background on the Cancer-Immunity Cycle

Immunity: Oncology Meets Immunology: The Cancer-Immunity Cycle

Clinical Cancer Research: Molecular Pathways: Next-Generation Immunotherapy—Inhibiting Programmed Death-Ligand 1 and Programmed Death-1