Primary and Secondary Immune Response
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Transcript of Primary and Secondary Immune Response
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Primary and Secondary Immune Response
1. When an individual is exposed to an antigenic substance, either by
injection, a complex series of events ensues,
a. An antigen-presenting cell (usually a macrophage) processes theantigen and presents it to the lymphoid cells of the immune system.
(1) For a successful immune response to occur, the processed
antigen (specifically, its epitope) must be presented to the
lymphocytes in association with a glycoprotein encoded by
genes of the major histocompatibility complex (MHC).
(2) This requirement for effective cell interaction is called MHC
restriction.
b. The lymphoid cells recognized that particular epitope and acquire the
ability to react with it.
c. The result of this sequence of events is the activation of antigen-
specific B and T cells, causing them to proliferate and mature.
2. The consequences of the initial interaction between
lymphocytes and their homologous epitopes are far-reaching.
a. A subsequent exposure to antigen will induce some B lymphocyte
(memory cells) to proliferate and differentiate into antibody-
secreting plasma cells.
(1) These active plasma cells release their specific antibody in
large amounts when they contact antigen a second time, a
phenomenon known as anamnesis.(2) The secreted antibody reacts specifically with the antigen that
originally induced the B cell to proliferate. The potential exists
to produce an extremely large (>100,000) variety of different,
specifically reactive, antibodies.
b. Some T lymphocytes (memory T cells) are induced to differentiate
and proliferate to form mature progeny that will be triggered to
release biologically active metabolites when they contact antigen a
second time.
c. Cells Involved In the Immune Response:
A. Macrophages:
Macrophages are versatile cells that play many roles. As scavengers, they rid the body of
worn-out cells and other debris. They are foremost among the cells that "present" antigen;
a crucial role in initiating an immune response. As secretory cells, monocytes andmacrophages are vital to the regulation of immune responses and the development of
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inflammation; they churn out an amazing array of powerful chemical substances
(monokines) including enzymes, complement proteins, and regulatory factors such as
interleukin-1. At the same time, they carry receptors for lymphokinesthat allow them tobe "activated" into single-minded pursuit of microbes and tumor cells.
After digesting a pathogen, a macrophage will present the antigen (a molecule, most
often a protein found on the surface of the pathogen, used by the immune system foridentification) of the pathogen to a corresponding helper T cell. The presentation is done
by integrating it into the cell membrane and displaying it attached to a MHC class II
molecule, indicating to other white blood cells that the macrophage is not a pathogen,despite having antigens on its surface.
Eventually the antigen presentation results in the production of antibodies that attach to
the antigens of pathogens, making them easier for macrophages to adhere to with their
cell membrane and phagocytose. In some cases, pathogens are very resistant to adhesionby the macrophages. Coating an antigen with antibodies could be compared to coating
something with Velcro to make it stick to fuzzy surfaces.
The antigen presentation on the surface of infected macrophages (in the context of MHC
class II) in a lymph node stimulates TH1(type 1 helper T cells) to proliferate (mainly duetoIL-12 secretion from the macrophage). When a B-cell in the lymph node recognizes
the same unprocessed surface antigen on the bacterium with its surface bound antibody,the antigen is endocytosed and processed. The processed antigen is then presented in
MHCII on the surface of the B-cell. TH1 receptor that has proliferated recognizes the
antigen-MHCII complex (with co-stimulatory factors- CD40 and CD40L) and causes theB-cell to produce antibodies that help opsonization of the antigen so that the bacteria can
be better cleared byphagocytes.
Macrophages provide yet another line of defense against tumor cells and body cells
infected with fungus orparasites. Once a T cell has recognized its particular antigen onthe surface of an aberrant cell, the T cell becomes an activated effector cell, releasing
chemical mediators known as lymphokines that stimulate macrophages into a more
aggressive form. These activated or angry macrophages, can then engulf and digestaffected cells much more readily. The angry macrophage does not generate a response
specific for an antigen, but attacks the cells present in the local area in which it was
activated.Macrophages are the major antigen-presenting cells of the body, interacting with antigen
as a primary step in the induction of an immune response. Langerhans cells of the skin,
dendritic cells, and B lymphocytes can also present antigen.
Besides presenting antigen to T and B cells, macrophages release soluble mediators suchas the monokine (macrophage-derived mediator with hormone-like effects) interleukin-1
(IL-1), which stimulates T cells to mature and to secrete lymphokines (lymphocyte-
derived mediators with hormone-like effects).
http://en.wikipedia.org/wiki/Monokinehttp://en.wikipedia.org/wiki/Interleukin-1http://en.wikipedia.org/wiki/Lymphokinehttp://en.wikipedia.org/wiki/Lymphokinehttp://en.wikipedia.org/wiki/Antigenhttp://en.wikipedia.org/wiki/Helper_T_cellhttp://en.wikipedia.org/wiki/Helper_T_cellhttp://en.wikipedia.org/wiki/Major_histocompatibility_complexhttp://en.wikipedia.org/wiki/Antibodyhttp://en.wikipedia.org/wiki/Velcrohttp://en.wikipedia.org/wiki/MHChttp://en.wikipedia.org/wiki/TH1http://en.wikipedia.org/wiki/TH1http://en.wikipedia.org/wiki/IL-12http://en.wikipedia.org/wiki/IL-12http://en.wikipedia.org/wiki/CD40http://en.wikipedia.org/wiki/Opsonizationhttp://en.wikipedia.org/wiki/Phagocyteshttp://en.wikipedia.org/wiki/Phagocyteshttp://en.wikipedia.org/wiki/Fungushttp://en.wikipedia.org/wiki/Parasitehttp://en.wikipedia.org/wiki/Parasitehttp://en.wikipedia.org/wiki/Lymphokinehttp://en.wikipedia.org/wiki/Interleukin-1http://en.wikipedia.org/wiki/Lymphokinehttp://en.wikipedia.org/wiki/Antigenhttp://en.wikipedia.org/wiki/Helper_T_cellhttp://en.wikipedia.org/wiki/Major_histocompatibility_complexhttp://en.wikipedia.org/wiki/Antibodyhttp://en.wikipedia.org/wiki/Velcrohttp://en.wikipedia.org/wiki/MHChttp://en.wikipedia.org/wiki/TH1http://en.wikipedia.org/wiki/IL-12http://en.wikipedia.org/wiki/CD40http://en.wikipedia.org/wiki/Opsonizationhttp://en.wikipedia.org/wiki/Phagocyteshttp://en.wikipedia.org/wiki/Fungushttp://en.wikipedia.org/wiki/Parasitehttp://en.wikipedia.org/wiki/Lymphokinehttp://en.wikipedia.org/wiki/Monokine -
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A macrophage of a mouse stretching its arms to engulf two particles,
possibly pathogens
Macrophage cell
Function of Macrophage cells:
1. These cells are actively involved in the engulfment and
destruction of various substances that enter the body.
2. They also are highly migratory and have the ability to
insinuate themselves into the small nooks and crannies of
the extracellular matrix of connective tissue.3. Macrophages ingest some large particular substances by
phagocytosis, a process that involves specific attachment
and ingestion. Also, they ingest dissolved solutes from their
fluid environment by pinocytosis.
a. Once a macrophage has adhered specifically to a
microorganism, it can ingest and destroy it. In certain
instances, cells such as lymphocytes will adhere
specifically to macrophages without being ingested.
b. Some macrophages, particularly those in the primary
alveoli, specialize in the nonspecific phagocytosis ofinspired particulate matter such as dust, pollen, and
cigarette smoke.
c. Specific phagocytosis involves coating
microorganisms with specific immunoglobulins or
complement factors- a process called opsonization-
and then adhesive recognition of bound
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immunoglobulins or complement factors by the cell
surface proteins of macrophages.
d. Ingested bacteria are destroyed by a mechanism that
probably is related to low lysosomal pH and the
presence of hydrolytic enzymes such as lysozyme.
4. Macrophages not only specifically ingest opsonized
microorganisms, they also can potentiate the lymphocyte
antibody production by binding certain antigens to their
surface and then interacting with lymphocytes to stimulate
antibody production.
5. Macrophages have the ability to migrate in a directed
fashion up a concentration gradient of dissolved components
of bacterial cell walls. This chemotactic behavior probably is
responsible for recruiting large numbers of macrophages to
areas of tissue destruction or infection.
Lymphocytes: The lymphocyte is a common leukocyte whose
heterogenous and complex nature was long misunderstood by
the histologists. Recent studies in cellular immunology,
however, have revealed two functional classes of lymphocytes :
B lymphocyte and T lymphocyte. Both lymphocyte types
originate from undifferentiated bone marrow stem cells.
a. B lymphocytes leave bone marrow and diffuse
throughout the body where they differentiate under
poorly understood inductive influences.
1. In birds, B lymphocytes differentiate in an organ
known as the bursa of Fabricus and thus are called
B cells.
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2. Although no structure equivalent to the bursa of
Fabricus has been clearly identified in any
mammal, even man, the name B cell is considered
as misnomer.
b. T lymphocytes or T cells leave bone marrow and
travel to the thymus where they differentiate.
Figure: Simplified
schematic of
humoral
immunity.
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Immune Response
Humoral
Immunity
Cell-mediated
Immunity
(Antibody) (Cytotoxicity)
http://www.cehs.siu.edu/fix/medmicro/hir.htmhttp://www.cehs.siu.edu/fix/medmicro/hir.htmhttp://www.cehs.siu.edu/fix/medmicro/cmir.htmhttp://www.cehs.siu.edu/fix/medmicro/cmir.htmhttp://www.cehs.siu.edu/fix/medmicro/hir.htmhttp://www.cehs.siu.edu/fix/medmicro/hir.htmhttp://www.cehs.siu.edu/fix/medmicro/cmir.htmhttp://www.cehs.siu.edu/fix/medmicro/cmir.htm -
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http://uhaweb.hartford.edu/BUGL/images/immbody.jpg -
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B cell development:a. In mammals, B cells originate from stem cells in the bone marrow.
b. During maturation, which also occurs in the bone marrow, the B cell
undergoes several gene rearrangements. These establish the B cells
antigenic specificity before it travels to secondary lymphoid organs.
Later somatic gene recombinations allow the cell line to switch from
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one immunoglobulin class to another without a change in antigenic
specificity.
c. When the B cell moves to the blood and peripheral lymphoid tissues,
it carries immunoglobulin in its surface membrane and is ready to
interact with antigen.
LYMPHOID TISSUES
Primary Secondary(Responsible for maturation of Ag-
reactive cells)(Sites for Ag contact and response)
Thymus
(T-cellmaturation)
Bone
marrow
Lymph
nodes
Spleen
(T-cell maturation) (B-cell maturation)
(Expansion oflymphatic system,
separate from bloodcirculation. Deepcortex harborsmostly T-cells,
superficial cortexharbors mostly B-
cells)
(Similar to lymphnodes but part ofblood circulation.Collects blood-
borne Ags)
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d. The B cell matures into one of two types of cells.
1. The plasma cells have abundant rough endoplasmic reticulum
and actively secretes large amount of the antibody that has been
anchored in the parent B cell membrane.
2. The memory B cell is a long-lived cell that is the progenitor
responsible for rapid plasma proliferation in the amnestic
response.
B-cell Function and Characterisatics:
1. B cells comprise approximately 35 percent of the circulating
lymphcytes and primarily are responsible for humoral
immunity (i.e., production of specific serum immunoglobulins
directed against various environmental antigens).2. B cells function in antibody production in two distinct ways.
a. In the first and clearly most simple case, antigens bind
directly to the B cells surface; B cells then undergo a
clonal proliferation followed by terminal differentiation
into plasma cells. Plasma cells are highly specialized for
the secretion of immunoglobulins.
b. In the second and more complex case, antigens are
bound to the surface immunoglobulins of helper T cells.
Next, these antigen-antibody complexes are released
from helper T cells and bound to macrophages. Finally,
the B cells interact specifically with stimulated
macrophages and subsequently undergo a clonal
proliferation and plasma cell differentiation.
3. Certain B cells persist after initial exposure to an antigen and
exist in the form of memory B cells. These cells can undergo a
rapid clonal expansion if a person is exposed again, even years
later, to the same antigen.
4. B cells are most heavily concentrated in the germinal centers of
aggregates of lymphoid tissue. For example, B cells are foundin large numbers in the cortical aggregates in lymph nodes and
in the white pulp of the spleen.
T cell development: Fetal stem cells are destined to become T
cells, which enter the thymus and proliferate there. These
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immature T cells (called thymocytes while in the thymus for the
periphery as mature T cells).
a. During T cell development in the thymus, several
changes occur.
1. Some type of selection process occurs, which favors the
proliferation of thymocytes that are restricted by self-
MHC molecules. That is, thymocytes are selected for
their ability to recognize antigens associated with
molecules of the same MHC type.
a. Precursors of both helperT (Th) cells (MHC
class II-restricted) and cytotoxic T (Tc)
lymphocyte (MHC class I- restricted) are
selected.
b. Current evidence suggests that cortical thymic
epithelial cells, which express both class I andclass II MHC glycoproteins are important in this
selection event; the mechanism is still unknown.
General Characteristics of T cells:
a. T cell surface markers:
1. Monoclonal antibody techniques have identified
molecules on the T cell membrane that function chiefly as
receptors.
2.These surface molecules include:
a. Class I and class II MHC molecules
b. Thy 1, Ly1, Ly2, 3 and L3T4 in mice.
c. CD (cluster of differentiation) antigens (e.g., CD3, CD4,
and CD8) in humans.
3. As a thymocyte differentiates toward a particular T cell
subtype, it acquires certain CD antigens in its membrane
and loses others. Thus, the T cell subsets can be
distinguished by their CD markers.
4. CD3, CD2, and CD5 are found on most peripheral blood
T cells.a. CD3 is a heteropolymer with at least five polypeptide
chains; it appears late in differentiation when the cells
are becoming immunocompetent.
i. CD3 is associated with the T cell receptor for
antigen and it is important in intracellular signaling
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to initiate an immune response once the cell has
interacted with a homologous epitope.
ii. CD3 is not directly involved in antigen
recognition, but antibodies against CD3 will block
the antigen-specific activation of T cells.
b. CD2 (the SRBC receptor) is responsible for
resetting of sheep red blood cells (SRBCs) in the
E-rosette assay for T cell enumeration.
c. CD5 is expressed on all T cells and on a subset of
B cells that appear to be predisposed to
autoantibody production.
5. CD4 and CD8 are present on different effector T cells
and on a subset of B cells that appear to be predisposed to
autoantibody production.
6. Antiserum against certain of the membrane markers (e.g.,against CD3) is immunosuppressive and has been used to
prevent rejection of transplanted tissues.
b. The T cell receptor for antigen
1. T cell have an antigen-specific receptor that functions as
the antigen-recognition site. This surface component, the T
cell receptor (TCR), bears significant structural homology
with the Fab portion of an antibody molecule.
2. Structure and Function of TCR:
a.The TCR is a heterodimer.
i. It consists of two nonidentical polypeptide chains, an
chain (about 45kDa) and a chain (about 40 kDa), linked
together by disulfide bonds.
ii. Both chains of the heterodimer are variable; there may be
more variability in the smaller () chain.
b. The TCR contains idiotypic determinants similar to those of
immunoglobulin molecules. Hypervariability occurs in
particular areas of each polypeptide chain in a manner
analogous to the complementarity-determining regions
(CDRs) of immunoglobulin molecules.c. The TCR heterodimer is noncovalently linked in the T cell
membrane to the ,, and chains of the CD3 molecule.
d. The TCR-CD3 complex apparently makes contact with both
the antigen and a portion of the MHC molecule. Different
portions of the hypervariable regions of the and chains
interact with:
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i. The helical sides of the epitope-binding cleft of the MHC
molecule.
ii. The epitope lying on the floor of the cleft.
e. CD4 or CD8 molecules (depending on the T
cell subset) also contact a portion of the MHC
molecule.
Primary and Secondary Immune Response:
a. The primary immune response occurs following the first exposure to
antigen and produces a relatively small amount of antibody.
b. If a sufficient length of time elapses after the primary antigenic
stimulation, the antibody level will decrease markedly.
c. However, subsequently exposure to even a small amount of antigen
will evoke an anamnestic response (also called booster response,memory response, or secondary immune response).
1. The anamnestic response consists of a rapid proliferation of plasma
cells, with the concomitant production of large amounts of specific
antibody.
2. The anamnestic response occurs because a
large population of memory B and T cells are recruited into the
humoral immune response.
a. These memory cells are produced during the initial exposure to
the antigen.
b. The memory cells are precursors of Th cells and plasma cells,
and represents another product of the collaboration between T
cells and B cells.
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Figure: Schematic Diagram of the Development of the Immune
Responses
Induction of primary immune responses
Induction of a primary immune response begins when an antigenpenetrates epithelial surfaces. It will eventually come into contact with
macrophages or certain other classes ofAntigen Presenting cells (APCs),
which include B cells, monocytes, dendritic cells, Langerhans cells and
endothelial cells. Antigens, such as bacterial cells, are internalized by
endocytosis and "processed" by the APC, then "presented" to
immunocompetent lymphocytes to initiate the early steps of the
immunological response. Processing by a macrophage (for example) results
in attaching antigenic materials to the surface of the membrane in
association with MHC II molecules on the surface of the cell. The antigen-
class II MHC complex is presented to a T-helper (TH2) cell, which is able
to recognize processed antigen associated with a class II MHC molecule on
the membrane of the macrophage. This interaction, together with stimulation
by Interleukin 1 (IL-1), produced by the macrophage, will activate the TH2
cell. Activation of the TH2 cell causes that cell to begin to produce
Interleukin 2 (IL-2), and to express a membrane receptor for IL-2. The
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secreted IL-2 autostimulates proliferation of the TH2 cells. Stimulated TH2
cells produce a variety of lymphokines including IL-2, IL-4, IL-6, and
gamma Interferon, which mediate various aspects of the immune response.
For example, IL-2 binds to IL-2 receptors on other T cells (which have
bound the Ag) and stimulates their proliferation, while IL-4 causes B cells to
proliferate and differentiate into antibody-secreting plasma cells and
memory B cells. IL-4 activates only B cells in the vicinity which themselves
have bound the antigen, and not others, so as to sustain the specificity of the
immune response.
Cross-linked antigens bound to antibody receptors on the surface of a B cell
cause internalization of some of the antigen and expression on the B cell
membrane together with MHC II molecules. The TH2 cell recognizes the
antigen together with the Class II MHC molecules, and secretes the various
lymphokines that activate the B cells to become antibody-secreting plasma
cells and memory B cells. Even if the antigen cannot cross-link the receptor,it may be endocytosed by the B cell, processed, and returned to the surface
in association with MHC II where it can be recognized by specific TH2 cells
which will become activated to initiate B cell differentiation and
proliferation. In any case, the overall B-cell response leads to antibody-
mediated immunity (AMI).
The antigen receptors on B cell surfaces are thought to be the specific
types of antibodies that they are genetically-programmed to produce. Hence,
there are thousands of sub-populations of B cells distinguished only by
their ability to produce a unique (reactive) type of antibody molecule. A B
cell can also react with a homologous antigen on the surface of the
macrophage, or with soluble antigens. When a B-cell is bound to Ag, and
simultaneously is stimulated by IL-4 produced by a nearby TH2 cell, the B
cell is stimulated to grow and divide to form a clone of identical B cells,
each capable of producing identical antibody molecules. The activated B
cells further differentiate into plasma cells, which synthesize and secrete
large amounts of antibody, and into a special form of B cells called memory
B cells. The antibodies produced and secreted by the plasma cells will react
specifically with the homologous antigen that induced their formation. Many
of these reactions lead to host defense and to prevention of reinfection bypathogens. Memory cells play a role in secondary immune responses.
Plasma cells are relatively short-lived (about one week) but produce large
amounts of antibody during this period. Memory cells, on the other hand, are
relatively long-lived and upon subsequent exposure to Ag they become
quickly transformed into Ab-producing plasma cells.
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Cell-mediated immunity
Generation of cell mediated immunity (CMI) begins when (for example)
a Tc cell recognizes a processed antigen associated with MHC I on the
membrane of a cell (usually an altered self cell, but possibly a transplanted
tissue cell or a eukaryotic parasite). Under stimulation by IL-2 produced by
TH2 cells the TC cell becomes activated to become a cytotoxic T
lymphocyte (CTL) capable of lysing the cell which is showing the new
(foreign) antigen on its surface, a primary manifestation of CMI.
The interaction between an antigen-presenting macrophage and a TH cell
stimulates the macrophage to produce and secrete a cytokine called
Interleukin-1 (IL-1) that acts locally on the TH cell. The IL-1 stimulates
the TH-cell to differentiate and produce its own cytokines (which in thiscase might be called lymphokines because they arise from a lymphocyte).
These lymphokines have various functions. Interleukin-4 has an immediate
effect on nearby B-cells. Interleukin-2 has an immediate effect on T cells as
described above.
Time is required before a primary immune response is effective as a host
defense. Antigens have to be recognized, taken up, digested, processed, and
presented by APCs; a few select TH cells must react with Ag and respond;
preexisting B or T lymphocytes must encounter the Ag and proliferate and
differentiate into effector cells (plasma cells or CTLs). In the case of AMI,
antibody level has to build up to an effective physiological concentration to
render its host resistant. It may take several days or weeks to reach a level of
effective immunity, even though this immunity may persist for many
months, or years, or even a lifetime, due to the presence of the antibodies. In
natural infections, the inoculum is small, and even though the antigenic
stimulus increases during microbial replication, only small amounts of
antibody are formed within the first few days, and circulating antibody is not
detectable until about a week after infection.
Induction of a secondary immune response
On re-exposure to microbial antigens (secondary exposure to antigen), there
is an accelerated immunological response, the secondary or memory
response. Larger amounts of antibodies are formed in only 1-2 days. This is
due to the activities of specific memory B cells or memory T cells which
were formed during the primary immune response. These memory cells,
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when stimulated by homologous Ag, "remember" having previously seen the
Ag, and are able to rapidly divide and differentiate into effector cells.
Stimulating memory cells to rapidly produce very high (effective) levels of
persistent circulating antibodies is the basis for giving "booster"-type
vaccinations to humans and pets.
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Immunoglobulin class switching:
a. The IgM-IgG switch.
1. In the primary immune response, the immunoglobulin produced
is mainly IgM. Subsequent exposures to the antigen will cause
the response to shift to IgG production.
2. This changeover occurs within individual plasma cells to
replace IgM-producing plasma cells.3. The individual plasma cell splices out the constant-region
gene complex and places it with a 3, 1, or another constant
region gene.
4. The entire light (L) chain gene complex and the variable,
diversity, and joining segments of the heavy (H) chain remain
intact. Thus, the antigenic specificity of the plasma cell and its
immunoglobulins is not changed.
b. Class switching to IgA, Ig D, or IgE takes place by similar splicing
processes.
Figure 4. Primary and Secondary Immune
Responses. Following the first exposure to an
antigen the immune response (as evidenced by
following the concentration of specific antibodyin the serum) develops gradually over a period of
days, reaches a low plateau within 2-3 weeks,
and usually begins to decline in a relatively short
period of time. When the antigen is encountered
a second time, a secondory (memory) response
causes a rapid rise in the concentration of
antibody, reaching a much higher level in the
serum, which may persist for a relatively long
period of time. This is not to say that a protective
level of antibody may not be reached by primary
exposure alone, but usually to ensure a high level
of protective antibody that persists over a long
period of time, it is necessary to have repeatedantigenic stimulation of the immune system.
Figure 3. Receptor
interactions between B
cells, T cells andAntigen Presenting
Cells (APC)
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Primary and Secondary Immune Responses
Primary Immune Response:
Following the first exposure to a foreign
antigen, a lag phase occurs in which no
antibody is produced, but activated B
cells are differentiating into plasma
cells. The lag phase can be as short as 2-
3 days, but often is longer, sometimes as
long as weeks or months.The amount of antibody produced is
usually relatively low.
Over time, antibody level declines to the
point where it may be undetectable.
The first antibody produced is manily
IgM (although small amounts of IgG are
usually also produced).
Secondary Immune Response :
If a second dose of the same antigen
is given days or even years later, an
accelerated secondary immune
response or anamnestic immune
response (IR) occurs. This lag phase
is usually very short (e.g. 3 or 4
days) due to the presence ofmemory cells.
The amount of antibody produced
rises to a high level.
Antibody level tends to remain high
for longer.
The main type of antibody produced
is IgG (although small amounts of
IgM are sometimes produced).
Note:The crossmatch attempts to prevent a secondary immune response bydetecting any antibody present, and then ensuring that only antigen-negative
red cells are transfused. It cannot prevent a primary immune response
because only autologous red cells or red cells from an identical twin will
introduce, no foreign antigens into a person being transfused.
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In blood banking, a primary immune response doesn't always cause mainly
IgM antibody to be produced. Sometimes only IgG antibody can be detected
(e.g., for antibodies in the Duffy or Kidd systems). Similarly, a secondary
immune response does not always cause mainly IgG antibody to be
produced. Sometimes, only IgM antibody is produced (e.g., for antibodies in
the MN or Lewis systems).