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I'm now going to turn to adaptive immunity.
So, we're talking about an overview of adaptive immunity, to begin with.
Our understanding of adaptive immunity came for the first time in
the 1890s when we had a brilliant scientist called Paul Ehrlich,
who figured out that somehow,
if foreign substances are put into vertebrates,
we can somehow make complementary molecules.
He called these complementary molecules.
So, the molecules that fit a lock to a key,
he called antibodies.
He even came out with a model of the immune system suggesting that
maybe we have cells with antibodies on the cell surface.
Then, when something foreign comes by and we call that an antigen,
when it triggers one of these cells,
the cell is then going to produce more of the same antibody.
So, this is a general view of immunity which got refined in
the 1950s by David Talmadge and Macfarlane Burnet,
is sometimes referred to as the clonal selection hypothesis.
So, imagine that we have many different immune cells
each with a different receptor.
An antigen comes by,
shown in green, binds to a specific cell-
binds to its receptor- triggers that cell,
and that cell then expands, as seen in the next view.
Now we have clonal expansion;
we have the expansion of all these cells all derived from
a single cell that recognizes a specific shape on this microbe, the antigen.
These expanded cells then differentiate.
In the case of B cells,
these would now secrete antibodies and the antibodies would now offer protection.
So, this overall picture of having individual cells each with different receptors, which
then respond to a specific antigen allowing the expansion of a single cell or a clone,
is the clonal selection hypothesis.