Antigen Presenting Cells (APCs)
383
Activation of
B cells
in T-cell area
Proliferation in
germinal center
Selection of
high-affinity B cells
via follicular DCs
B-cell
differentiation
Plasma
cell
Germinal
center
T-cell
B-cell
Follicular DC
Memory
B-cell
T cell
B cell
B-cell
clones
IL-2
IL-4
IL-5
CD28 CD80
CD40L CD40
CD28 CD80
CD40L CD40
IL-2, IL-4
Antigen
Fig. 9
T cell–B cell interactions outside and inside germinal centers: B cells
encountering activated T cells in the T-cell areas of a lymph node are stimulated via
cytokines to proliferate and form the germinal center. Binding to follicular DCs, which
present native antigen, leads to selection of high-afFnity B cells. The B cells that have
survived reencounter activated T cells thereby receiving a differentiation signal. This
gives rise to antibody-secreting plasma cells and memory B cells.
The peptide that is generated by proteolytic
digestion of the antigen, bound and pre-
sented by MHC class II molecules, and
recognized by a CD4
+
T cell is termed
‘‘
T-cell epitope
.’’ It is a linear epitope.
In the majority of cases, B- and T-cell
epitopes are distinct entities with different
functions. This can be nicely illustrated
with hapten–protein conjugates: hapten-
speciFc B cells bind the hapten via the
BCR, which mediates efFcient internaliza-
tion. This means that the hapten contains
the B cell epitope. The hapten, how-
ever, cannot be bound by MHC class II
molecules. This is why a carrier protein
is necessary: the T-cell epitope to be pre-
sented to CD4
+
T cells is a peptide derived
from the carrier protein. The requirement
for MHC-associated presentation of the T-
cell epitope for T-cell activation accounts
for the MHC restriction of B cell–T cell
interactions.
Which mechanisms prevent B cells that
do not possess an antigen-speciFc BCR but
are localized close to an antigen-speciFc B
cell, from so-called
bystander activation
?
There are several characteristics of the
B cell–T cell interactions that counteract
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