primary and secondary immune response

7/29/2019 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
http://en.wikipedia.org/wiki/Mousehttp://en.wikipedia.org/wiki/Mouse


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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
http://uhaweb.hartford.edu/BUGL/images/immune-duality.jpg


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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).

primary and secondary immune response

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