I love summer! I love riding my bike when it's hot. More
than that, I love riding my bike with Andrew in tow. Andrew and I recently rode
out the Foothills Trail between Orting and South Prairie. We found a little picnic area next
to a pond where we feasted on peanut butter sandwiches and homemade cookies and
then sat together watching frogs, tadpoles, and dragonflies.
My garden seems to love the hot weather too. I spend most of
my weekends working in my garden while neglecting this blog.
One of my reasons to discussing the different types of
immune responses to vaccines is to use this as a basis for discussing different
types of vaccines, why some vaccines are much more effective than others, why
some vaccines require "booster" doses and others do not, and why some
vaccines contain adjuvants.
In my last post I gave an overview of innate immunity; skin, mucous membranes,
and stomach acid that act as barriers to foreign invaders, complement
that tears holes in cells that are not recognized as self, and white blood
cells that kill infected cells and others that eat pathogens. Although the goal of immunization is to stimulate adaptive
immune responses, antigen-presenting cells, which are part of innate immunity, are
integral to adaptive immunity.
Antibodies
Adaptive immunity develops after the immune system
encounters a foreign antigen – something that is non-self. One of the most
important parts of adaptive immunity is antibodies.
As we saw in The Fantastic Voyage, antibodies attach to foreign invaders.
Specifically, antibodies attach to antigens.
Each antibody attaches to a specific antigen. By attaching to antigens on the
surface of a pathogen, the antibody can block the pathogen from attaching to
its target cell and prevent it from killing or invading that cell. Antibodies
can also help phagocytic white blood cells engulf and destroy a pathogen. For
example, a number of pathogenic bacteria are covered with a polysaccharide
capsule – they are literally sugar-coated – which protect them from
phagocytosis. Antibodies can attach to polysaccharide epitopes, giving the
phagocytic cell something to grab onto.
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| NIAID/Jeanne Kelly |
B-lymphocytes
B-lymphocytes,
also known as B-cells, are the workhorse of adaptive immunity. B-cells
transform into plasma cells and manufacture antibodies. The surface of B-cells
is covered with B-cell receptors (BCR). These are essentially antibodies that
are anchored to the cell membrane. Each B-cell receptor is made to attach to a
specific non-self antigen, which is known as its cognate antigen; the
antigen it "recognizes." Of course, a B-cell cannot see if its
cognate antigen is actually attached to a pathogen, so it needs more
information before it commits to cloning itself to make enough plasma cells to
fight off an attack. One way is when there are many B-cell receptors on the surface
of the B-cell engaged with many cognate antigens on the surface of a pathogen.
Another is when there is a chemical messenger from other cells that tells the B-cell that there is a battle
going on and its antibodies are needed. Sometimes B-cells need some help.
T-lymphocytes
There are a lot of different types of T-cells.
For this discussion, I'm just going to talk about helper T-cells. Helper
T-cells interact with B-cells in several different ways. A B-cell can enlist
the help of a T-cell to determine whether it needs to differentiate into a plasma
cell and make antibodies. T-cells can help B-cells make antibodies that are a
better fit for the target antigen and they also help with immune memory. Helper
T-cells also act as intermediaries between antigen-presenting cells and
B-cells; an antigen-presenting cell brings the antigen to a helper T-cell that
then attaches to a B-cell to "teach" it to make antibodies to that
antigen.
While B-cells "recognize" many different types of
molecules, helper T-cells only recognize protein antigens. That means that
antibody responses to antigens that are not proteins, like polysaccharides, are
T-cell independent; the antibodies do not "fit" as well as those
made during T-cell dependent responses and immune memory is not as robust – it takes
the immune system longer to remember that it has previously fought a battle
with the pathogen and it takes longer to mount an antibody response than with
T-cell dependent responses.
Incidentally, the human immunodeficiency virus (HIV) kills
helper T-cells. Symptoms
of acquired immunodeficiency syndrome (AIDS) appear when there are not enough helper T-cells to fight
off opportunistic infections.
Cell-mediated immunity
Helper T-cells that have been activated by antigen-presenting
cells can "teach" other types of white blood cells to recognize and kill
infected cells. Cell-mediated immunity is one of the reasons live virus
vaccines are highly effective.
Again, this is a simple explanation of very complex
processes that I plan to use as a basis for discussions on a number of
vaccines.
Thanks to all of my readers for 20,000 pageviews!
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