primary and secondary immune response

Date:6/26/2021 www. qadricohs.edu.pk FB Page: Qadri College of Health Sciences, Karachi, Sindh, Pakistan. 1
QADRI COLLEGE OF HEALTH SCIENCES, KARACHI
U-3, 5 OF 5
“DEFENSE MECHANISMS OF THE BODY”
By: Aftab H. Abbasi
RN, DCHN, BSN, MA, LL.B
Lecturer Nursing
Qadri College of Health Sciences Karachi

“DEFENSE MECHANISM OF THE BODY”
- This unit focuses on the resistance of the
body which microorganism’s encounter
where they enter in the human body.
- This unit highlights the importance of the
resistance or defense of the body which
will help learners in understanding that
why infection occurs sometimes and not
always.

At the completion of this unit learners will
be able to:
1- Explain the role of good health in protection against the microbial
infection.
2- Define Resistance and Susceptibility.
3- Define Nonspecific Resistance.
4- Describe the role of the skin and mucous membrane in nonspecific
Resistance.
5- Explain the process of Phagocytosis.
6- Define the Specific Resistance, Innate Resistance and Immunity.
7- Explain four types of acquired Immunity.

At the completion of this unit learners will be
able to:
8- Differentiate between humoral and cell mediated immunity.
9- Define Antigens, hapten and antibodies.
10- List the five classes of antibodies and their functions.
11- Explain the role of memory, tolerance and specificity in immunity.
12- Distinguish between primary and secondary immune response.
13- Define Hypersensitivity.
14- Differentiate between i.e. delayed and immediate Hypersensitivity.

12- PRIMARY AND SECONDARY IMMUNE RESPONSE
Differences between Primary and Secondary
Immune Response:
In a primary immune response, naive B cells are
stimulated by antigen, become activated, and
differentiate into antibody-secreting cells that
produce antibodies specific for the eliciting
antigen.
A secondary immune response is elicited when the
same antigen stimulates memory B cells, leading
to the production of greater quantities of specific
antibodies that are produced in the primary
response. Some of the differences between
Primary and Secondary Immune Response are
as follows:

S.N. Characteristics
Primary Immune
Response
Secondary Immune
Response
01. Definition Primary Immune
Response is the reaction
of the immune system
when it contacts an
antigen for the first time.
Secondary Immune
Response is the reaction of
the immune system when it
contacts an antigen for the
second and subsequent
times.
02. Appearance Appears mainly in the
lymph nodes and spleen.
Appears mainly in the bone
marrow and then, in the
spleen and lymph nodes.
03. Occurrence This occurs in response
to the primary contact of
the antigen.
This occurs in response to
the second and subsequent
exposure to the same
antigen.
04. Antibody Peak The antibody level
reaches its peak in 7-10
days.
The antibody level reaches
its peak in 3-5 days.

Primary Immune
Response
Secondary Immune
Response
05. Affinity of Antibody Low affinity to their
antigens.
High affinity to their
antigens.
06. Responding Cells Naive B cells and T
cells
Memory B cells
07. Antibodies Both thymus-
dependent and
thymus-independent
antibodies are
involved in the
primary immune
response.
Only thymus-dependent
antibodies are involved in
the secondary immune
response.
08. Lag Phase Long (4-7 days) Short (1-4 days)

Primary Immune
Response
Secondary Immune
Response
09. Types of
Antibodies
A large amount of IgM
and a small amount of
IgG are produced
during the primary
immune response.
A large amount of IgG, a
small amount of IgM, IgA,
and IgE are produced
during the secondary
immune response.
10. Amount of
Antibody
Few antibodies are
produced in the
primary immune
response.
100-1000 times more
antibodies are produced in
the secondary immune
response.
11. Strength of the
Response
The primary immune
response is usually
weaker than
secondary immune
response.
The secondary immune
response is stronger.

Primary Immune
Response
Secondary Immune
Response
12. Antibody level
Antibody level declines
to the point where it
may be undetectable.
The antibody level tends to
remain high for longer.
References:
http://www.microbiologynotes.com/differences-between-primary-and-secondary-immune-response/

13- Define Hypersensitivity
Hypersensitivity (Immunological reaction)
refers to:
- Undesirable immune reactions produced by
the normal immune system.
Hypersensitivity reactions:
- When an immune response result in
exaggerated OR in appropriate reactions
harmful to the host the term hypersensitivity
OR allergy used.

13- Define Hypersensitivity
Hypersensitivity reactions:
Four types; based on the mechanisms
involved and time taken for the reaction, a
particular clinical condition (disease) may
involve more than one type of reaction.
Classification of Hypersensitivity:
- Type I Type I, II and III Antibody Mediated
- Type II
- Type III
- Type IV Type IV Cell Mediated

Type I (Immediate) Hypersensitivity
- Commonly called allergy.
- Mediated by IgE antibodies produced by plasma
cells in response to stimulation of Th2 cells by an
antigens.
- The antigens that stimulate it are called allergens
(i.e. House dust, Pollens, Cosmetics, Insects,
Clothing and Drug).
- Exposure may be ingested, inhalation, injection or
direct contact.
- Type I hypersensitivity reactions can be systemic
(e.g., systemic anaphylaxis) or localized to a
specific target tissue or organ (e.g., allergic
rhinitis, asthma).

Type II (Cytotoxic) Hypersensitivity
- Cytotoxic
- Type II hypersensitivity involves IgG or
IgM antibody-mediated.
- IgM or IgG immunoglobulin react with cell-
surface antigens to activate the
complements system and produce direct
damage of the sell surface.
- Transfusion reactions and hemolytic
disease of the newborn are examples of
type II hypersensitivity.

Type III (ICM) Hypersensitivity
Type III (Immune Complex–Mediated) Hypersensitivity:
- Type III hypersensitivity is also known as immune
complex hypersensitivity.
- The reaction may take 3 - 10 hours after exposure to
the antigen (as in Arhus reaction).
- The reaction may be general (e.g., serum sickness)
or may involve individual organs including or other
organs.
- Antigens causing immune complex mediated injury
are:
Exogenous
Endogenous

Type IV (Cell Mediated) Hypersensitivity
Type IV (Delayed or Cell-Mediated) Hypersensitivity:
- Delayed hypersensitivity is a function of T Lymphocytes, not
antibody.
- It starts hours (or Days) after contact with the antigen and
often lasts for days.
- It can be transferred by immunologically committed
(Sensitized) T cells, not by serum.
- Principal pattern of immunologic response to variety of intra
cellular microbiologic agents
i.e.: Mycobacterium Tuberculosis
Viruses
Fungi
Parasites

Hypersensitivity Reactions Conclusion:

14- Delayed VERSUS immediate Hypersensitivity
Immediate hypersensitivity:
Immediate hypersensitivity (type I) is also
known as immediate contact urticaria or
contact urticaria syndrome, and the reaction
occurs very rapidly.
Common causes include insect bites and
ingested peanuts. It is mediated by IgE
antibodies, which bind to the surface of mast
cells. Within minutes of skin contact by an
antigen, the mast cells release histamine and
other factors, causing an inflammatory
reaction.

Immediate Hypersensitivity
Anaphylaxis is an extreme form of immediate
hypersensitivity. It is a life-threatening reaction
involving massive histamine release, which can
lead to breathing difficulties and low blood
pressure.
Instance of anaphylaxis due to skin contact
from an essential oil or constituent.
There is also recorded cases of anaphylactic
shock from fragrance inhalation.

Delayed VERSUS immediate Hypersensitivity
Delayed Hypersensitivity:
Type IV hypersensitivity reaction also known as cell mediated
hypersensitivity or delayed type of hypersensitivity is the T
lymphocytes mediated destruction of cells along with dendritic cells,
macrophages and cytokines playing major roles.
The reaction is mediated by specific subsets of CD4+ helper T cells
(Th-1 and Th-17 cells) or by CD8+ cytotoxic T cells.
Type IV hypersensitivity occurs 24 hours after contact with an
antigen, usually starting at 2 or 3 days and often last for many
days.
For this reason, type IV hypersensitivity reaction is termed as
“delayed hypersensitivity”.
Type IV hypersensitivity is unique in that, unlike the first three types
of hypersensitivity which are antibody mediated, type IV
hypersensitivity is cell mediated and also a delayed reaction.

Here is the comparison table:
1- Alternative Name:
Type I Type II Type III Type IV
Allergic
hypersensitivity
Cytotoxic
hypersensitivity
Immune
complex
hypersensitivity
Cell-mediated
hypersensitivity/
Delayed type of
hypersensitivity
2- Principle:
Antibody-mediated
degranulation of
granulocytes
leading to the
destruction of
cells.
Antibody-mediated
destruction of
healthy cells.
Antigen-antibody
complex-mediated
destruction of
cells.
T lymphocytes
mediated the
destruction of
cells.

3- Primary Mediator:
IgE IgG/IgM IgG/IgM
Specific subsets
of CD4+ helper
T cells or CD8+
cytotoxic T cells.
4- Other components as mediators:
Immediate or within
a few hours
5-8 hours 2-8 hours
After 24 hours only,
mostly 48-72 hours
after contact
Mast cells, Basophils,
histamine & other
pharmacological agents
Complement,
Neutrophils
Complement,
phagocytes and K cells
Dendritic cells,
macrophages, and
cytokines
5- Reaction time:

6- Antigen:
Free in circulation
(Soluble)
Fixed on cells
Free in circulation
( Soluble)
Soluble or cell-
bound
7- Antigen origin:
Exogenous
Endogenous or
exogenous
Exogenous or
endogenous
Exogenous or
endogenous
8- Antibody:
Fixed on mast cells
and basophils
Free in circulation Free in circulation Not applicable

9- Mechanism:
Allergen-specific
IgE antibodies
bind to mast cells
via their Fc
receptor. When
the specific
allergen binds to
the IgE, cross-
linking of IgE
induces
degranulation of
mast cells.
IgG or IgM
antibody binds to
a cellular antigen,
leading to
complement
activation and cell
lysis. IgG can also
mediate ADCC
with cytotoxic T
cells, natural killer
cells,
macrophages, and
neutrophils.
Antigen-antibody
complexes are
deposited in
tissues.
Complement
activation provides
inflammatory
mediators and
recruits
neutrophils.
Enzymes released
from neutrophils
damage tissue.
Th2 cells secrete
cytokines, which
activate
macrophages and
cytotoxic T cells.

10- Complement activation:
No Yes Yes No
11- Appearance:
Weal & flare Lysis & necrosis
Erythema &
edema
Erythema &
induration
12- Transfer with serum:
Passive transfer
possible with
serum
Passive transfer Passive transfer
Cannot be
transferred with
serum; but
possible with T
cells transfer

13- Desensitization:
Easy but short-
lived
Easy but short-
lived
Easy but short-
lived
Difficult but long-
lived.
14- Examples:
Asthma, Rhinitis,
Atopic eczema,
Bee sting reaction
Rhesus
incompatibility (Rh
hemolytic
disease),
Transfusion
Reactions, Cell
Destruction due to
autoantigens,
Drug-Induced
Hemolytic Anemia
Glomerulonephriti
s, Systemic Lupus
Erythematosus,
Farmer’s lung
arthritis, Vasculitis
The tuberculin
reaction,
Granuloma
formation, Allergic
contact dermatitis,
Type-1 diabetes

References:
• https://courses.lumenlearning.com/microbiology/chapt
er/hypersensitivities/
• http://www.biologydiscussion.com/immunology/4-main-
types-of-hypersensitivity-immunology/61851
• https://www.slideshare.net/drsomeshwaranamsana/hy
persensitivity-reactions-dr-somesh-microbiology
• http://www.yourarticlelibrary.com/immunology/type-iii-
hypersensitivity-and-its-mechanism-human-
immunology/28081
• Lydyard, P.M., Whelan,A.,& Fanger,M.W.
(2005).Immunology (2 ed.).London: BIOS Scientific
Publishers.
• Owen, J. A., Punt, J., & Stranford, S. A. (2013). Kuby
Immunology (7 ed.). New York: W.H. Freeman and
Company.

11- Role of memory, tolerance and specificity in immunity
Specificity, Memory and Tolerance:
- Specificity refers to the adaptive immune
system's ability to target specific pathogens.
- Memory refers to its ability to quickly
respond to pathogens to which it has
previously been exposed.
- Tolerance, also referred to as immunological
tolerance or immunotolerance, is an active
state of unresponsiveness to specific
antigens in an effort to prevent destructive
over-reactivity of the immune system.

DEFENSE MECHANISMS OF THE BODY

By: Aftab H. Abbasi
RN, DCHN, BSN, MA, LL.B
Lecturer Nursing
Qadri College of Health Sciences Karachi

primary and secondary immune response

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