Chapter 11: Vaccines

Why is boosting important?

More than one vaccination with the same vaccine may be required because protection is not permanent. It is necessary to recruit more B cells to produce the antibodies to remind existing sensitized B cells to continue to make antibodies.

Vaccines with inactivated organisms

Contains organisms that could cause disease but have been killed or inactivated, preventing them from reproducing and causing disease.

Vaccines with inactivated organisms examples

Flu vaccine, cholera vaccine, hepatitis A vaccine

Attenuated vaccines

Contain live organisms but have been modified so that they no longer reproduce or cause disease. They still retain their unique code, however.

Attenuated vaccines examples

Measles, mumps, rubella, and polio

Toxoids vaccines

Contain either a modified toxin that an organism produces or an actual part of the organism. In either case, the toxoid has the unique antigen code.

Toxoid vaccine examples

Tetanus, diphtheria, whooping cough, and HPV

Biosynthetic vaccines

A type of vaccine that contains science-made substances that are similar to the parts of an organism that causes disease

Biosynthetic vaccine examples

Hib

mRNA vaccines

Lab-made pieces of genetic material that code for making a specific part of an organism. For example, the Covid-19 spike on the outside of the virus. The mRNA is taken by the human cells and begins to make part of the virus, then makes antibodies to the spike protein.

mRNA vaccine example

Only type of mRNA vaccine is made for the Covid-19 virus.

Why is antibody mediated immunity considered short-term immunity?

The body recognizes the antibodies as foreign and attacks them quickly, so it is mainly used for patients with little to no active immunity.

Artificial acquired passive immunity is most used to prevent…

severe disease or death from tetanus, rabies, and snake venom.

RhoGAM, or anti-Rh antibodies

Administered to women who are Rh-negative and have just given birth to an Rh-positive baby. This prevents the mother's immune system from making large amounts of anti-Rh antibodies, as they kill the Rh-positive cells before the mother's immune cells can become sensitized to them.

Autoantibodies

Antibodies produced against self-antigens

How does the immune system affect the joints with rheumatoid arthritis?

The helper T-cell stimulates B-cells to produce autoantibodies directed against cartilage and other connective tissues of the joint. The helper T's also increase production of a variety of mediators that also attack joint tissues, thus changing the joint anatomy and destruction of these tissues.

Traditional drugs for rheumatoid arthritis

systemic corticosteroids, NSAIDs, and DMARDs

Why are traditional drugs sometimes not ideal for rheumatoid arthritis?

-Systemic corticosteroids and NSAIDs are helpful in reducing some of the pain and inflammation but it does not control the abnormal immune system responses and does not prevent progressive tissue destruction.
-DMARDs temporarily slow progressive destruction by suppressing cell division of WBCs, however DMARDs are high-alert drugs with many serious side effects

How does biologic immunosuppressive therapy work?

Some of these antibodies target specific mediator molecules or their receptors. Another antibody type targets an intracellular enzyme, Janus kinase, which functions to promote signaling systems that increase the growth and function of almost all immune system cells and their products.

How do monoclonal antibody biologics work to treat autoimmune disorders?

It is a TNF inhibitor that binds to and prevents TNF from triggering cell and tissue destruction. Also inhibits the release of other cytokines. This reduces inflammation and immune functions that trigger the production of autoantibodies.

What mediator is most involved in rheumatoid arthritis joint destruction?

tumor necrosis factor of TNF

Cytokines

small signaling proteins secreted by immune cells that act as chemical messengers to regulate immunity, inflammation, and blood cell production

Why are monoclonal antibodies given parenterally?

The antibodies can be denatured in the GI tract

What are Janus Kinase enzymes?

Enzymes present in regulatory immune cells, especially lymphocytes. When mediators and cytokines bind to lymphocyte receptors, JAKs transmit the activation signals from the lymphocyte's membrane to its nucleus, which then turns on the genes to synthesize many cytokines that will increase the growth and activity of nearly all WBC's. JAK activation increases all inflammatory pathways and mediators, including TNF and autoantibodies, and increases immune attacks.

How do Janus Kinase inhibitors work?

Work by binding to JAKs to prevent the transmission of signals to the nucleus of immune cells. Fewer inflammatory mediators and cytokines are available to maintain autoimmune responses.

JAK inhibitors are…

All oral drugs and prescribed after other drugs, like direct-acting monoclonal antibodies, did not provide relief. These drugs are classified as target specific DMARDs.

How do general antirejection drugs work?

T-cells are most responsible for attacking and destroying transplanted organs. These drugs work by selective immunosuppression, suppressing only the immune cells responsible for organ rejection, and placing the recipient at less risk for developing severe infection

What combo of drugs is used to prevent organ rejection?

corticosteroids, DMARDs, and selective immunosuppressants.

How does the selective immunosuppressive mycophenolate work to prevent organ rejection?

Inhibits an enzyme needed for lymphocyte production. Also prevents T cells from being activated.

How does the corticosteroid, prednisone, work to prevent organ rejection?

It suppresses production of WBCs in bone marrow to inhibit immune responses

How does the calcineurin inhibitor, tacrolimus, work to prevent organ rejection?

Prevents the first phase of T-cell activation by binding to protein and forming a complex that inhibits calcineurin present in some immune cells, as calcineurin promotes T cell division and activation

Acute transplant rejection

Despite daily antirejection therapy, periods of increased immune attack may occur throughout life

Therapy for acute episodes

the same general antirejection drugs are used but at temporary higher doses. Some may be given IV during the episode. Monoclonal and polyclonal antibodies may be used temporarily for 10-14 days to provide additional help.

Acute rejection monoclonal antibodies help by…?

Stopping T-cell functions by targeting a receptor on activated T-cells and does not affect other types of immune cells. They must be given IV

Acute rejection polyclonal antibodies help by…?

Attacks and eliminates T-cells and can lead to profound immunosuppression. Only for acute rejection episodes after kidney transplantation

Polyclonal antibodies are produced by..

other animal cells (like horse and rabbit cells) being exposed to human T cells

Monoclonal antibodies are produced by..

mouse cells or a combo of mouse and human antibody-producing cells