IMMUNITY
Dr. Binu Babu
Asso. Professor
Mrs. Jincy Ealias
Assi. Professor

Immunity
• The term immunity refers to the body’s specific
protective response to an invading foreign agent or
organism.
• The human body has the ability to resist almost all
types of organisms or toxins that tend to damage
the tissues and organs. The capability is called
immunity.

Types of immunity

INNATE IMMUNITY ADAPTIVE IMMUNITY
• Resistance to infection which
individual possesses by virtue
of his genetic and
constitutional make up
• Early defense response against
microbes
• Immune response Non specific
• Innate response do not alter on
repeated exposure
• Memory effect absent
• Not affected by immunization
or prior contact
• The resistance that an
individual acquires during life
• Later defense response
• Immune response is highly
specific
• Adaptive response improves
with each successive
encounter with same pathogen
• Memory effect present
• Is improved by immunization

Natural (Innate immunity)
• The basis of natural defense mechanisms is the
ability to distinguish between self and non-self.
• Such natural mechanisms include
1. Physical and chemical barriers
– Skin and mucous membrane
– Antimicrobial substance in body secretions
2. The action of WBCs
3. Inflammatory response.

Classifications of Innate immunity
Innate
Immunity
Species Racial Individual

Species immunity
• Refers to the total or relative refractoriness to a
pathogen, shown by all members of species.
• Person obtains by virtue of being a part of the human
species.
• Determines whether or not a pathogen can multiply in
them.
Example
• All human beings are totally unsusceptible to plant
pathogens and to many animal pathogens, such as
render pest or distemper.
• Pasteur’s experiments on anthrax in frogs, which are
naturally resistant to the disease but become susceptible
when their body temperature is raised from 25° to 35°C.

Racial immunity
• Racial differences are known to be genetic in origin
Example
• People of Negroid origin in USA are more
susceptible than the Caucasians to tuberculosis.
• Genetic resistance to Plasmodium falciparum
Malaria seen in some parts of Africa and
Mediterranean coast.
• A hereditary abnormality of red cells (sickling)
prevalent in the area, confer immunity to infections
by malarial parasite.

Individual immunity
• The difference in innate immunity exhibited
by different individuals in a race
• The genetic basis of individual immunity is
seen in twins.
Example
• Homozygous twins exhibit similar degrees
of resistance or susceptibility to
Lepromatous leprosy and Tuberculosis.

Determinants of innate immunity
1. Species and strains
2. Age
3. Hormonal Influences
4. Nutrition

MECHANISMS OF INNATE
IMMUNITY
1. Epithelial surfaces
• Skin
• Mucosa of the respiratory tract
• Human eye.
• Flushing action of urine
2. Antibacterial substances in Blood and tissues
3. Inflammation
4. Fever
5. Cellular factors

ACQUIRED IMMUNITY
 A person is said to be immune when he possesses specific
protective antibodies or cellular immunity as a result of
previous infection or immunization or is so conditioned by
such previous experience as to respond adequately to
prevent infection.
 This form of immunity develops as a response to infection
and is adaptive to the infection, it is called adaptive
immunity.
 The characteristics of adaptive immunity are
 Specificity for distinct molecules.
 An ability to remember and respond more vigorously to repeated
exposure to the same microbe. Hence it is also called as specific
immunity.

• Natural Active immunity
– This results from either a clinical or inapparent
infection.
– Immunity following chicken pox and measles infection
is usually life long
• Artificial Active Immunity
– This is the resistance induced by vaccines.
– Vaccines are preparations of live or killed
microorganisms or their products used for
immunization.

Naturally acquired passive
immunity
• This is the resistance passively transferred from the
mother to the baby. In human infants, maternal
antibodies are transmitted predominantly through the
placenta.
• Human colostrums, which is also rich in IgA antibodies
and resistant to intestinal digestion.
• Synthesis of antibodies (IgM) occurs at 20th week of
IUL but its immunogenic capacity is still inadequate at
birth. It is only by about the age of three month that
the infants acquire a satisfactory level of
immunological independence.

Naturally acquired active
immunity
• Naturally acquired active immunity occurs
when a person is exposed to a live pathogen,
and develops a primary immune response,
which leads to immunological memory

Artificially acquired passive
immunity
 Artificially acquired passive immunity is a short-term immunization
induced by the transfer of antibodies, which can be administered in
several forms; as human or animal blood plasma, as pooled human
immunoglobulin for intravenous (IVIG) or intramuscular (IG) use, and in
the form of monoclonal antibodies (MAb).
 This is the resistance passively transferred to a recipient by
administration of antibodies.
 Passive immunization is indicated for immediate and temporary
protection in a non-immune host
 Employed for the suppression of active immunity, when the latter may
be injurious.
 Used as treatment of some infections.
 Hyper immune sera of animal or human origin, convalescent sera and
pooled human gamma globulins are used for prophylaxis and therapy.
 Rh immune globulin is used during delivery to prevent immune response to
the Rhesus factor in Rh-negative women with Rh-positive babies.

Artificially acquired active
immunity
• Artificially acquired active immunity can be
induced by a vaccine, a substance that
contains antigen. A vaccine stimulates a
primary response against the antigen
without causing symptoms of the disease.

ACTIVE IMMUNITY PASSIVE IMMUNITY
1. Produced actively by host’s immune
system
Received passively by the host
2. Induced by infection or by contact
with immunogens (vaccines,
allergens etc).
No participation by the host’s immune
system
3. Affords desirable and effective
protection
Conferred by introduction of readymade
antibodies
4. Immunity effective only after a lag
period (time required for generation
of antibodies).
Protection transient and less effective
Immunity effective immediately
5. Immunological memory present;
subsequent challenge more
effective (booster effect)
No immunological memory subsequent
administration of antibodies less
effective due to immune elimination
6. Negative phase may occur No negative phase
7. Not applicable in immunodeficient
hosts
Applicable in immunodeficient hosts

• Inactivated vaccines are composed of micro-organisms that
have been killed with chemicals and/or heat and are no
longer infectious. Examples are vaccines
against flu, cholera, plague, and hepatitis A.
• Live, attenuated vaccines are composed of micro-
organisms that have been cultivated under conditions
which disable their ability to induce disease.
– Examples include yellow fever, measles, rubella, and mumps.
• Toxoids are inactivated toxic compounds from micro-
organisms in cases where these (rather than the micro-
organism itself) cause illness, used prior to an encounter
with the toxin of the micro-organism.
– Examples of toxoid-based vaccines include tetanus and diphtheria.
• Subunit vaccines are composed of small fragments of
disease causing organisms. A characteristic example is the
subunit vaccine against Hepatitis B virus

Types of Vaccine:
• Immunizing agents that are used for immunoprophylaxis
 Bacterial vaccines:
– Live (BCG vaccine for T.B.).
– Killed (Cholera vaccine).
– Subunit (Typhoid Vi antigen).
– Bacterial products (Tetanus Toxoid).
 Viral Vaccine:
– Live (Oral polio vaccine – Sabin).
– Killed (Injectable polio vaccine – Salk).
– Subunit (Hepatitis B-vaccine).
 Combinations
• If more than one kind of immunizing agent is included in the
vaccine, it is called a mixed or combined vaccine.
• DPT (Diphtheria – pertussis - tetanus)
• MMR (Measles, mumps and rubella).
• DPTP (DPT plus inactivated polio).

Physical and chemical barriers
Skin and mucous membrane
• When skin and mucous membrane are intact and
healthy they provide a physical barrier to invading
microbes.
• Sebum and sweat secreted on to the skin surface
contains antibacterial and antifungal substances.
• Hairs in the nose acts as a filter.
• One way flow of urine from the bladder during
micturition

Antimicrobial substance in body
secretions
1. Hydrochloric acid in gastric juice
2. Lysosomes
3. Saliva
4. Immunoglobulin in nasal secretions and saliva
5. Interferons

White blood cell action
• WBCs participate in both the natural and the
acquired immune responses.
• Granulocytes include neutrophils, eosinophils and
basophils.
• Nongranular leucocytes include monocytes or
macrophages and lymphocytes.
• Lymphocytes consisting of B cells and T cells, play
major role in humoral and cell mediated immune
responses.

Inflammatory response
• Major function of the natural (non specific or
innate) immune system.
• Chemical mediators assist this response by
minimizing blood loss, walling off the invading
organism, activating phagocytes and promoting
formation of fibrous scar tissue and regeneration
of injured tissue

Dysfunction of the natural immune system
• Immunodeficiency
• Persistent inflammatory response
• Autoimmune bodies

Response to invasion
• When the body is invaded or attacked by bacteria,
viruses, or other pathogens, it has three means of
defending itself:
1. The phagocytic immune response
2. The humoral or antibody immune response
3. The cellular immune response

Phagocyte immune response
• The first line of defense
• Involves the WBCs (granulocytes and
macrophages), which have the ability to
ingest foreign particles.
• Phagocytes also remove the body’s own
dying or dead cells.

Humoral immune response
 A second response, the humoral immune response
(sometimes called the antibody response), begins
with the B lymphocytes, which can transform
themselves into plasma cells that manufacture
antibodies.
 The third mechanism of defense, the cellular
immune response, also involves the T
lymphocytes, which can turn into special cytotoxic
(or Killer) T cells that can attack the pathogens
themselves.

Humoral immune response
1. Before exposure to a specific antigen, the clones of B
lymphocytes remain dormant in the lymphoid tissue.
2. On entry of a foreign antigen, macrophages in the
lymphoid tissue phagocytize the antigen and then present
it to adjacent B lymphocytes.
3. Those B lymphocytes specific for the antigen immediately
enlarge and take on the appearance of lymphoblasts.

Humoral immune response cont…
4. Some of the lymphoblasts further differentiate to
form plasmablasts, which are precursor of
plasma cells.
5. The mature plasma cells then produces gamma
globulin antibodies.
6. Other B lymphocytes differentiate into B-
lymphocyte clones with a memory for the
antigen.

Primary response and secondary response
Primary response
1. Response for forming
antibodies that occur on
first exposure to a specific
antigen.
2. Appears 1 week after,
with weak potency and
short life
Secondary response
1. Response that occurs
after second exposure to
the same antigen.
2. Begins rapidly after
exposure to the antigen
(often within hours) is far
more potent (energy),
and forms antibodies for
many months rather than
for only a few weeks.

Role of antibodies

Antibodies
The antibodies can inactivate the invading agent in one of the
several ways, as follows:
1. Agglutination: in which the multiple large particles with
antigens on their surface.
2. Precipitation: in which the molecular complex of soluble
antigen and antibody becomes so large that it is rendered
insoluble and precipitates.
3. Neutralization: in which the antibodies cover the toxic
sites of the antigenic agent.
4. Lysis: in which some potent antibodies are occasionally
capable of directly attacking membranes of cellular agents
and thereby cause rupture of the agent.

Types of immunoglobulin

IgG
IgG (75% of total immunoglobulin)
 Appears in serum and tissues (interstitial fluid)
 Assumes a major role in bloodborne and tissue
infections.
 Activates the complement system.
 Enhances phagocytosis
 Crosses the placenta

IgA
IgA (15% of total immunoglobulins)
 Appears in body fluids (blood, saliva, tears, breast
milk, and pulmonary, gastrointestinal, prostatic
and vaginal secretions).
 Protection against respiratory, gastrointestinal and
genitourinary infections.
 Prevents absorption of antigens from food.
 Passes to neonate in breast milk for protection.

IgM
IgM (10% of total immunoglobulins)
• Appears mostly in intravascular serum
• Appears as the first immunoglobulin produced in
response to bacterial and viral infections.
• Activates the complement system.

IgD
IgD (0.2% of immunoglobulins)
 Appears in small amounts in serum
 Possibly influences B-lymphocytes differentiation ,
but role is unclear.
IgE
IgE (0.004% of immunoglobulins)
 Appears in serum
 Takes part in allergic and hypersensitivity of
reactions
 Combats parasitic infections.

Cellular immune response
• These develop gradually over a period of 24 to 48
hours after the second encounter with an antigen.
• T lymphocytes are primarily responsible for
cellular immunity.
• Stem cells continuously migrate from the bone
marrow to the thymus gland, where they develop
into T cells.
• By spending time in the thymus, these cells are
programmed to become T cells rather than
antibody producing B lymphocytes.

Cellular immune response cont…
• T cells attack foreign invaders directly. Cellular
reactions are initiated by the binding of an antigen
with an antigen receptor .
• The T cells then carry the antigenic message, or
blue print, to the lymph nodes, where the
production of other T cells is stimulated.
• Some T cells remain in the lymph nodes and retain
a memory for the antigen. Other T cells migrate
from the lymph nodes into the general circulatory
system and ultimately to the tissues.

Types of T cells
1. Helper T cells:
• When activated, helper T cells secrete cytokines
that attract and activate B cells, cytotoxic T cells,
natural killer cells, macrophages and other cells
of the immune system.
• Helper T cells produce different types of
cytokines and determine whether the immune
response will be the production of antibodies or
cell mediated immune response.

2. Cytotoxic T cells
• Cytotoxic T cells is a direct attack cell that is
capable of killing micro-organisms and, at times,
even some of the body’s own cells.
• For this reason these are called killer cells.
• Cytotoxic attack the antigen directly by altering
the cell membrane and causing cell lysis and
releasing cytolytic enzymes and cytokines.

3. Supressor T cells
• They are capable of suppressing the functions of
both cytotoxic and helper T cells.
• It is believed that these suppressor functions
serve the purpose of preventing the cytotoxic cells
from causing excessive immune reactions that
might be damaging to the body’s own tissues.

Complement system
• Circulatory plasma proteins which are made in the
liver and activated when an antibody couples with
its antigen, are known as complement.
• Complement has three major physiological
functions:
a. defending the body against bacterial infection
b. bridging natural and acquired immunity
c. Disposing (placing) of immune complexes and the
byproducts associated with inflammation.

Complement system
Complement mediated immune response are summarized as:
1. Cytolysis: Lysis and destruction of cell membranes of
body cells or pathogens.
2. Isonization: Targeting of the antigen so that it can be
easily engulfed and digested by the macrophages and
other phagocytic cells.
3. Chemotaxis: chemical attraction of neutrophils and
phagocytic cells to the antigen.
4. Anaphylaxis: activation of mast cells and basophils with
release of inflammatory mediators that produce smooth
muscle contraction and increased vascular permeability.

Abnormal immune reactions
1. Antibody mediated
2. Cell-mediated
3. Mixed antibody

Antibody mediated reactions
• These occur within minutes of exposure to an
allergen (antigen).
• The most common manifestations of this type of
allergic reaction include: food allergies, childhood
eczema, hay fever, extrinsic asthma.
• In these conditions the released chemicals act
locally, causing different effects that depend on the
site.

Acute systemic anaphylaxis (anaphylactic shock)
• It is caused by the entry of an allergen into the
blood e.g. snake venom, injectable penicillin.
• There are profound effects throughout the body,
including generalized vasodilatation, leading to
severe hypotension and contraction of smooth
muscle in the respiratory tract, causing acute
breathing difficulties.

Other antibody mediated reactions:
• Reaction of antibodies with cells that have
antigens on their cytoplasmic membranes may
cause the cells to rupture.
• Abnormal reactions to antibody/antibody
complexes sometimes result in them adhering to
the endothelium of blood vessels causing
inflammation and local damage.
.

Cell mediated reactions
The antigen include:
1. Intracellular microbes, e.g. those causing
tuberculosis, measles, mumps.
2. Some vaccines, e.g. against smallpox.
3. Some metals and compounds that combine with
protein in the skin and cause allergic contact
dermatitis.

Mixed reactions
Autoimmune diseases:
• Tissue damage and signs of disease as the body fails to
recognize its own tissues. Destruction of the body’s
own cells may be either humoral or cell-mediated.
– Thyroid- Hashimoto’s thyroiditis
– Stomach- Addisonian pernicious anemia
– Cortex of the adrenal gland- addison’s disease.
– Pancreas-type I diabetes mellitus
Organ transplantation and rejection
• GVHD

Health education
• About the signs and symptoms that indicate
infection.
• Whenever they experience a symptom that
is not typical for them, they should contact
their health care provider.
• About any prophylactic medication regimen,
including dosage, indications, times, actions,
and side effects.
• Avoid others with infections and crowds.

Health education cont…
 The patient and family also need to learn about
other ways to prevent infection.
 Instructed to monitor for subtle changes in
physical status and must be informed of the
importance of seeking immediate health care if
changes occur.
 About the importance of continuing the treatment
regimen and assisted in incorporating it into their
lives.

References
1. Wilson KJW, Waugh A. Ross and Wilson Anatomy and
physiology in Health and illness. Eigth edition. NewYork;
Churchill Livingstone:1998.
2. Smeltzer SC, Bare B. Textbook of Medical surgical Nursing.
10th edition. Philadelphia; Lippincott Williams and
wilkins: 2004.
3. Guyton AC, Hall JE. Textbook of Medical Physiology.
Eleventh edition. Philadelphia; Saunder (Elsevier) : 2006.