Because lymphocytes recombine their antigen receptor
genes in a random way, it means that we can produce
millions and millions and millions of different
B-cell receptors on the surface of B-cells;
and millions and millions of different
T-cell receptors on the surface of the T-cells.
So that’s great, means that whatever
pathogen comes along, if some
new pathogen arises or if an existing pathogen undergoes mutation
and changes its antigens, we should have some lymphocytes that
have an antigen receptor specific for that particular pathogen.
However, that comes at a price.
This huge diversity of T-cells and huge
diversity of B-cells means that for any
given single pathogen, we don’t have
millions and millions and millions of cells.
We may only have a few
hundred or a few thousand.
It’s actually not enough to do the
job of getting rid of the infection.
So there’s a problem there.
So how does the immune system
get around that problem?
Well, it does it by clonally selecting
the B-cells and the T-cells that are
required, then activating them and causing
them to divide and divide and divide.
So that particular
specificity will expand up.
So rather than having just a few thousand, let’s say T-cells
and B-cells against Streptococcus for example; rather than just
having a few thousand, you
end up with millions, and that is
enough to do the job that’s needed to eliminate the infection.
So clonal selection of lymphocytes is key to the way
in which the adaptive immune response functions.
So here we have a B-cell in the middle, say five different
B-cells with five different specificities of B-cell receptor.
And this one is specific for that
particular virus that we can see there.
And it will become activated by the mechanisms that we’ve just
reviewed, and part of that activation
will initiate cell proliferation.
The cell will divide and it will divide and
it will carry on dividing multiple times.
And expand up the number of cells so that a sufficient
number is generated to eliminate the particular infection.
Once the cells become activated, not only do
they proliferate, but they also differentiate.
So a naïve B-cell, one that has not
previously encountered the antigen,
if it encounters the antigen it’s
specific for, it will become activated.
As part of that activation, proliferation
will be induced following clonal selection.
And then the B-cell can differentiate
down one of two different pathways.
Most of the B-cells will
develop into plasma cells.
These are the antibody secreting
version of the B-cell.
So a B-cell will differentiate
into a plasma cell.
It has a rather different
appearance to the B-cell.
It has more cytoplasm, which is
why it’s called a plasma cell.
It has lots of rough endoplasmic reticulum which
is the place where proteins are made in cells.
And this particular cell is going to make lots and lots and
lots and lots of one particular protein, the antibody molecule.
So these plasma cells can now secrete vast amounts of antibody
against the antigen that initially
stimulated that particular B-cell.
So if this B-cell was against Cytomegalovirus, you’ll
produce lots of antibody against Cytomegalovirus.
However not all of the B-cells
differentiate into plasma cells.
Some of them will differentiate
into memory B-cells.
And these cells are crucially important
in developing a secondary immune response.
Characteristic feature of the
adaptive immune response is that upon
a subsequent encounter with the same
antigen, the response is much faster.
And actually, not only is it faster but the
quality of the response is much better as well.
And this property depends upon
the generation of memory B-cells.
So memory B-cells provide the basis
of the secondary immune response.
Looking here on this graph, we can see the magnitude of the
response following the first encounter with a given antigen.
The adaptive immune response develops
this primary immune response.
This term primary and secondary immune response there,
it’s uniquely used for the lymphocyte responses.
It’s characteristic of
the adaptive response.
We don’t see this in
the innate response.
The innate response is the same however
many times the antigen is encountered.
But here we see a
adaptive immune response.
And initially the primary
immune response, it’s okay.
But it doesn’t make masses of antibody that… not masses of
T-cells are produced, but it usually
is sufficient to do the job.
But on a second encounter with the same
antigen, because during the first response
memory cells were generated, the second
response gets off the ground much faster.
It goes to a much higher level
and it stays up for much longer.
So both qualitatively and quantitatively, secondary immune
responses are superior to primary immune responses.