Vaccines: How they train the immune system to protect you from infections

Dr. Daniel Remick

A nurse administers a vaccine in a girl’s deltoid. Photo courtesy of Centers for Disease Control and Prevention.

How can a needle jabbed into your arm protect you from a virus that enters through your nose?
This article explains the basic immunology driving your response to a vaccine so that you are protected from infections.

A few definitions:

• Antigens: molecules that your immune system recognizes as dangerous so they will be blocked or removed. Most pathogens (bacteria and viruses) have many antigens.

• Antibodies: immune molecules that recognize specific antigens.

Vaccines mimic how an infection trains your immune system. After an infection, such as a head cold, you produce antibodies and T cells (more to come) that protect you from future infections.
Your immune response has great specificity, so protection against a virus that causes the first infection does not protect against a second, unrelated virus that can also cause a cold. Vaccines train the immune system to provide defense against a specific virus or bacteria, which explains why there are different vaccines.

B cells are lymphocytes that originate in the bone marrow. The antigens in the vaccine migrate to the local lymph nodes to activate the B cells. Their primary role is to secrete antibodies.

Each B cell has a unique protein on the cell surface that only recognizes one antigen. An analogy is a lock and key, where the key is the antigen and the lock is the antigen receptor. When the antigen, e.g. a pathogen molecule, binds to its unique receptor that B cell becomes activated and secretes antibodies. These antibodies bind to the antigens and neutralize the pathogen.

For example, antibodies to the virus that causes COVID-19 lock onto a spike protein on the outside of the virus. The antibody prevents the virus from entering your cells and protects you from infection.
T cells develop in a specialized organ called the thymus, a small organ in your chest. Each T cell has a unique antigen receptor on the cell surface, similar to the B cells.

Specialized cells at the vaccination site bring the vaccine antigens to the local lymph nodes where the T cells become activated. There are two major classes of T cells, T helper cells and cytotoxic T cells.
T helper cells provide help to other immune cells by releasing mediators, i.e. signals that help B cells make better antibodies. Among these mediators are cytokines.

You may see ads for cytokine inhibitors used to treat autoimmune diseases such as rheumatoid arthritis or psoriasis. Sometimes these ads warn that if you should tell your doctor if you plan to receive a vaccine since blocking the cytokines may prevent the vaccine from being fully effective.

Cytotoxic T cells. If the pathogen has already invaded your normal cells, cytotoxic T cells kill these virally infected cells. Killing normal but virally infected cells eliminates the reservoir of infection in your body. For example, if a virus has invaded into the normal cells in the lining of your nose, the cytotoxic T cells will destroy these cells.

Memory cells develop after the first vaccination or infection, including both B cells and T cells. These cells are primed so that when they detect the pathogen again they quickly leap into action to prevent an infection.

Let’s put this all together. After getting the vaccine in your arm some antigen moves to the local lymph node and activates B cells to make antibodies. Antigens also activate T helper cells that help B cells make better antibodies and Cytotoxic T cells kill host cells infected with a pathogen.

Some people feel ill after receiving a vaccine and mistakenly believe that the vaccine gave them an infection. What actually occurred is that the immune response to the vaccine causes some mild symptoms similar to an infection, such as a low-grade fever or the chills.

Rest assured that a flu shot will not give you the flu.

Daniel Remick, M.D. is Professor Emeritus of Pathology & Laboratory Medicine at the Boston University Chobanian and Avedisian School of Medicine and former Chair of that Department. Prior to moving to Boston, he was a Professor of Pathology and Assistant Dean of Admissions at the University of Michigan. His research has been supported by grants from the NIH for more than three decades. Dr. Remick grew up in Duluth and graduated from Central High school in 1971.