section 35.2
Acquired or Adaptive Immunity
complement proteins to be activated so that they can
attack and lyse invading microbes or signal phagocytic
cells to destroy the invaders. Complement activation that
occurs in response to antigen-antibody complexes oc-
curs via the “classical pathway” of complement acti-
Acquired immunity is dependent on the presence of
low levels of antibodies that recognise antigens of the in-
fecting organism, phagocytic cells that respond to anti-
body tagged antigens, and memory B cells that are poised
to produce large quantities of antibodies to the infecting
agents. Memory B cells live for long periods and respond
quickly with enhanced antibody production upon reinfec-
tion with organisms or foreign agents that have been pre-
viously encountered. Some T cells also possess memory
and are similarly poised for rapid response should a re-
encounter with the same antigen occur. Immunological
memory, involving both B cells and T cells, is the mech-
anism that makes vaccination effective and explains why
an individual does not become ill a second time when ex-
posed to the same pathogens, e.g., the pathogens that cause
measles or whooping cough.
Infectious agents such as viruses and other microbes
(e.g., mycobacteria), as well as parasites, enter the host
cells or are engulfed by macrophages and become in-
accessible to attack by B cells and antibodies. Lysoso-
mal (endosomal) enzymes of the infected host cells de-
grade the components of the infecting organism. The
resulting degradation products (e.g., peptides), bound to
specialized host cell proteins, are transported to the ex-
ternal surface of the cell where they are presented to
the extracellular milieu bound to specialized host cell
membrane proteins. The proteins that bind these antigen
degradation products are components of the
major his-
tocompatibility complex (MHC),
HLA system.
capable of presentation of peptides of the infectious organ-
isms are described as “antigen-presenting cells” (APCs).
The group of MHC proteins involved in presentation of
antigen by macrophages and by B cells are members of
“class II” MHC proteins. The antigen-presenting cells
with digestion products from the invading agent now
bound to their external surfaces attract CD4+ T lym-
phocytes (
T-helper cells)
capable of recognizing the de-
graded pieces of the antigen from the infectious organ-
ism. The T-helper cells produce protein messengers or
effector molecules (cytokines). Cytokines provided by
the T cells “direct” the differentiation of B cells to form
plasma cells and memory cells and also initiate mecha-
nisms that result in inactivation of the virus. Cytokines
also signal other specific T lymphocytes, thus preparing
them to respond to the infectious organism(s). Recog-
nition occurs between the MHC II-presented molecules
on the APC and an antigen (epitope)-specific T-cell re-
ceptor (TcR). The TcR molecules are, like antibodies,
specific for the antigen (e.g., epitopes on the peptides)
and for the particular MHC protein. The recognition of
molecules presented by MHC II proteins involves another
T-cell membrane protein, CD4 (cluster differentiation pro-
tein 4). The immune response that involves B cells and
MHC class II antigen presentation is schematically illus-
trated in Figure 35-1 and that which involves macrophages
and MHC class II antigen presentation in shown in
Figure 35-2.
Nucleated cells other than those specific to the immune
system process infectious agents such as viruses somewhat
differently from the MHC II mechanism. For example,
viral DNA or RNA replication within the host cells results
in the production of new virus, including viral proteins.
These newly synthesized viral proteins are degraded to
peptides within the infected cell and are bound to an MHC-
related carrier protein. The bound peptides are transported
to the endoplasmic reticulum and subsequently to the ex-
ternal surface of the cell membrane. Recognition of the
degraded pieces of the infectious agent again occurs via
proteins of the MHC system proteins; however, in this case
it is with proteins of the “class I” MHC. The presentation
of the viral protein-derived peptides on the surface of the
cell labels the cell as infected and makes it a target for
A second group of T cells, CD
cytotoxic T cells
quently abbreviated CTLs or Tc cells), are similar to CD4+
T cells in that each type of T cell clone interacts only with
a particular peptide epitope presented by MHC proteins.
Cytotoxic T cells bind to and kill the marked, infected
cells via specific TcRs. These T cells undergo clonal pro-
liferation to create many additional T cells that are spe-
cific for the particular epitopes that the MHC I protein
presents and only that T-cell clone recognizes. Among
theses T cells are some that persist for a long time and
thus become “memory” T cells, poised to prevent later
infection by the same agent. These T cells release the cy-
tokine, intcrfcron-y, which prepares other cells to resist
and destroy the invading virus. Cytotoxic T cells and their
TcRs also act in conjunction with another membrane pro-
tein, CD
. Cellular immune response that involves almost
any “ordinary” cell and MHC class I antigen presentation
is shown schematically in Figure 35-3.
The cells that are the principal agents of adaptive or
acquired immunity are from the lymphoid lineage of stem
cells. Similar to the situation with myeloid cells, mutations
in lymphoid precursor cells give rise to the
In summary, acquired immunity is a lymphocyte-
dependent (B and T cell) process by which molecular prop-
erties of infectious agents are recognized, anti-infectious
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