IMMUNITY

 Ability to resist
almost all types of
organisms or toxins
that tend to damage
the tissues and
organs.
 Two types - innate immunity
- acquired immunity
 It is present at birth – inborn immunity

 Invariable hereditary response

 Also called natural or native immunity

 It is present through out life

 Independent of
previous exposure
to disease causing
agents or foreign
substances

 No specificity, no
memory

 Non specific immunity

 The cells that mediate innate immunity –
neutrophils, macrophages, natural killer
cells.

 Epithelial cells & endothelial cells also

contribute innate immune response.
 Innate immunity includes the following :

1. Phagocytosis of bacteria and other

invaders by WBC & cells of tissue
macrophage system

2. Destruction of swallowed organism by the

acid secretion of the stomach & the
digestive enzymes.
3. Resistance of the skin to invasion by
organisms.

4. Urinary tract is protected from infections by

the washing action of the urine.
5. Presence in the blood of certain chemical
compounds like

 lysozyme – mucolytic polysaccharide that

causes bacteria to dissolute.

 Basic polypeptides – inactivate certain types

of gram positive bacteria.
 Also called adaptive immunity or specific
immunity

 Powerful immunity when attacked by

microorganisms
 The body recognizes these agents by specific
proteins or polysaccharides in their make up.

 These are called antigens.

 INNATE IMMUNITY
Inborn immunity - since birth
Early phase of host response
without requiring prior
exposure
Non specific – general
protection
Immediate, integrates with
adaptive immune system
Does not alter on repeated
exposure
No memory
ACQUIRED IMMUNITY
Acquired after birth
Late phase response of
antigen specific lymphocytes
to antigens
Specific for a particular
pathogen
Lag time b/w exposure and
maximal response
Improves with each exposure
Immunological memory
present
 Cell mediated or T- cell immunity

 by activated T lymphocytes.

 Major defense against

 Infections by viruses,fungi and few

bacteria like tubercle bacilli

 Delayed allergic reactions & rejection of

transplanted tissues
 Humoral immunity

 By the activation of B lymphocytes.

 Also called B cell immunity.

 Secrete antibodies into the blood and lymph.

 Eg: defense against bacterial & viral

infections.
 Acquired immunity is of 2 types :
natural
active
artificial

natural
passive
artificial
 Resistance developed as a result of an
antigenic stimulus.

 Active functioning of host’s immune

apparatus.

 More effective.

 Better protection.
 Due to clinical or subclinical infection by a
microbe.

 Eg : a person who has recovered from

measles develops this type of immunity.

 It is life long lasting.

 Induced by vaccines.

 Vaccines are preparations of live or killed

microorganisms or their products used for
immunisation.
 It is transmitted passively to a recipient in a
readymade form.

 Immune system plays no active role.

 No antigenic stimulus; preformed antibodies

are given.
 Less effective ; inferior to active
immunity

 Main advantage - immediate action

 Transfer of antibodies from mother to fetus
through placenta.

 Human breast milk (colostrum) which is rich

in IgA antibodies gives protection to the
neonate.
 Resistance passively transferred to a
recipient by the administration of antibodies
activated T lymphocytes, or both

 Obtained from the blood of some animals

that has been immunised against the antigen
 Eg: Tetanus immunoglobulin, rabies
immunoglobulin

 The antibodies last in the body of the

recipient for 2-3 weeks .

 These are used for prophylaxis & therapy.

ACTIVE IMMUNITY PASSIVE IMMUNITY

Production of antibodies in Transfer of antibodies in readymade

response to antigens form – no involvement of immune
system
Negative phase – Ag combining No negative phase – as antigens are
with preexisting Ab and lowering not injected
their level
Latent period – for generation of No latent period
antibodies

Secondary response – due to Absent

immunological memory

Long lasting Short lasting

More effective, better protection Less effective

Not applicable in immunodeficient Applicable in immunodeficient

individuals individuals
 Mediated through
activated T Lymphocytes.

 There are 4 types of T lymphocytes :

1. Helper T cells
2. Suppressor T cells Regulatory T cells
3. Cytotoxic T cells
4. Memory T cells
 They form 3/4 th
of T lymphocytes.

 Major regulator of all immune functions.

 This is by forming a series of protein mediators

called lymphokines or cytokines

 Eg: - IL 2, IL 4, IL 5, IL6, GMCSF, Interferon γ etc.

 IL 2 : stimulates growth & proliferation of
cytotoxic and suppressor T cells

 IL 2 : direct positive feed back effect in

stimulating helper T cells themselves.
IL 2, IL 4, IL 5, IL6 : stimulate B cell growth
and differentiation to form plasma cells and
antibodies.
 they help in humoral immunity.

 IL 2 & interferon γ : activate macrophages

and cause them to accumulate in the
inflamed tissue area.
 There are 2 subtypes of helper T cells.

1. T helper 1 cells (TH1 cells) –

 secrete IL 2 & IFN γ
 concerned with cellular immunity.

2. T helper 2 cells (TH2 cells) –

 secrete IL 4, IL 5, IL6
 interact primarily with B cells in
relation to humoral immunity
 Most helper T cells display the glycoprotein
marker CD4.

 So they are also called CD4 T cells

 Markers on the surface of lymphocytes are

assigned CD (clusters of differentiation)
numbers on the basis of their reaction to a
panel of monoclonal antibodies
CYTOTOXIC T CELLS
 It is a direct attack cell that is capable of
killing microorganism or even body’s own
cells.

 So they are called killer cells.

 Cytotoxic T cells bind to the antigen on
cells or microorganisms with the help of
receptors

 After binding they secrete hole forming

proteins, perforins

 They produce holes in the membrane of

the attacked cell.
 Fluid flows rapidly in to the attacked cell
from interstitial space
 Cytotoxic T cells release cytotoxic &
digestive enzymes in to the attacked cell
and destroy it.

 They kill virus particles, cancer cells and

transplanted cells

 Development cytotoxic T cells is aided

by helper T cells by secreting IL 2
 They display the glycoprotein marker CD8.So
they are called CD8 T cells
 They suppress the functions of cytotoxic T
cells and helper T cells, B cells and
macrophages
 They prevent the cytotoxic T cells from
causing excessive immune reaction against
body’s own tissues.

 Thus they help in immune tolerance

 Suppressor T cells along with the
helper T cells are called regulatory T
cells.

 Growth & proliferation of suppressor T

cells is stimulated by helper T cells.
Memory T cells

 After exposure to a given antigen, a small no.

of activated T cells persist as memory T cells.

 These cells are readily converted to effector

cells by a later encounter with the same
antigen.
 This ability to produce an accelerated
response to a second exposure to antigen
is a key feature of acquired immunity

 The ability persists for long time

 In case of measles, it can be life long.

 Dendritic cells in the lymph nodes and
spleen - most potent

 Langerhan’s dendritic cells in the skin

 Macrophages.

B cells.
DENDRITIC
CELLS
 Antigen entering the host is phagocytosed
and degraded

 Peptide fragment of antigen presented

along with major histocompatibility
antigens (MHC antigens) on the surface of
antigen presenting cell (APC)
 Antigens present on cell membrane of cells

 Encoded by genes : histocompatibility

genes

 Collectively constitute
major histocompatibility complex
 These genes are located on the short arm of
of chromosome 6.

 MHC proteins are also called Human

Leucocyte Antigens (HLA).

 They are glycoproteins.

 Divided into two.
1. Class I MHC protein ( MHC I protein or HLA
class I)
 Present on all the cells of body except RBCs

 Activate T8 cells

 CD8 act as coreceptor

 Coupled to intracellular antigens

2. Class II MHC protein (MHC II protein or HLA
Class II)

 present only on immunologically

active cells like activated T cells, B cells,
macrophages, and other antigen presenting
cells.
 Concerned with peptide products of extra-
cellular antigens like bacteria.

 Activates T4 cells, coreceptor –CD4

MHC class III protein

 For complement components of classical

and alternative complement pathway
 B Cells directly bind antigen

 T cells : have antigenic recognition receptors

called TCR (T cell receptor)

 Specific surface receptors

 Recognize and interact with an antigenic

determinant on the antigen
 A multi subunit complex

 Two disulfide linked polypeptide chains, α and

β chains that mediate antigen recognition

 The T cell receptors are surrounded by

adhesion proteins
 Adhesion proteins bind to complementary
protein on the APC to form the ‘immunologic
synapse’

 This permits T cell activation to occur

 2 signals are necessary to produce T cell

activation.
 One is produced by binding of the digested
antigen to the cell receptor.

 Other is produced by the joining of the

surrounding proteins in the ‘synapse’.
I. An antigen-presenting cell
ingests and partially digests an
antigen (mostly virus)

 It presents part of the antigen

along with MHC peptides on its
surface
Partially digested
antigen
II. IL -1 secreted by APC activates
CD4 T cell

 An "immunologic synapse"
forms with a CD4 T cell, which is
activated to produce IL-2
T CELL
APC
III. IL-2 acts in an autocrine fashion
to cause the helper T cell to
multiply, forming a clone
 Meanwhile, the virus may infect epithelial
cells

 Within the infected epithelial cells, the virus

is processed

 The partially digested antigen attached to

MHC class I protein & presented on the cell
surface
 Activated CD4 cell activates cytotoxic
CD8 T cell.

 This cell recognises & binds MHC class I-

antigenic peptide complex on infected
epithelial cells
 Cytotoxic T cells cause lysis of infected
epithelial cells

 When the viral infection is controlled, the

activated cytotoxic T cells are turned off by
suppressor T cells
 Some activated cytotoxic T cells become
memory T cells

 They respond quickly if second attack

occurs
1. Protection against fungi, viruses and
intracellular bacterial pathogens

2. Graft rejection

3. Delayed hypersensitivity reaction

4. Associated with certain autoimmune
disorders

5. Immunity against cancer

 Mediated by circulating immunoglobulin
antibodies in the γ globulin fraction of the
plasma proteins.

ACTIVATED ‘ B’ CELLS

MEMORY B CELLS PLASMA CELLS

IMMUNOGLOBULINS
Mechanism
 When the antigen first enters the body,
it binds directly to the receptors on B
cells.

 The antigen is presented to the T cells

at the same time and activated helper T
cells are formed
 These helper T cells are needed to
produce full activation of B cells and
antibody formation

 The TH2 cells secrete cytokines- IL4,

IL5, IL6 that stimulate B cell growth
and differentiation in to plasma cells
 Some of the activated B cells proliferate
and transform in to memory B cells

 So subsequent exposure to the same

antigen will cause much more rapid &
much more potent antibody response
 The plasma cells secrete
immunoglobulins

 The immunoglobulins are secreted form

of antigen binding receptors on the B
cell membrane
 Each immunoglobulin (Ig) contain 4 polypeptide
chains.

 Two identical long chains are called heavy chains

 Two identical short chains are called light chains

 There are 2 types of light chains – κ and λ

 There are 8 types of heavy chains

 A molecule of Ig may have either κ or λ

chain, but never both together.

 The chains are joined by disulfide bridges

Each chain has

 a variable segment in which aminoacid

sequence is highly variable

 a constant portion in which aminoacid

sequence is constant.

 Variable segment form the antigen binding

site
 The constant portion determines biological
properties of antibody

1. diffusivity of antibody in the tissues

2. adherence of the antibody to the specific

structures within the tissues

3. attachment to the complement complex etc.

 The heavy chain has 2 other segments.

1. Diversity (D) segment – AA sequence is

highly variable.

2. Joining segment (J) – AA sequence is

moderately variable.
Each Ig is divided into 2 fragments.

 Fab fragment (fragment antigen binding) –

is the fragment with which the antigen
combines.

 It is made up of entire light chain and part of

the heavy chain.

 Antigen combines at the amino terminal of

the Ig.
 A constant region fragment called
Fc fragment (fragment crystallisable)

 It is made up of only heavy chain

 This portion has binding sites for

complement and macrophage

 It is involved in biologic function of Ig.

 It is the effector portion which mediates the
reaction initiated by antibodies.

 Based on the nature of their heavy chains,

they are divided into 5 main classes.

1. IgG
2. IgM
3. IgA
4. IgE
5. IgD
 Major serum Ig - 80% of the total

 Four subclasses – IgG1, IgG2, IgG3, IgG4

 Only maternal Ig that is normally transported

across the placenta & provides natural
passive immunity in the new born.

 It forms the main secondary antibody

response
 IgM
 Ig with highest mol.wt.

 pentamer (all others are monomers)

 earliest Ig to be synthesised by the

fetus beginning about 20 weeks of age.
 Not transported across the placenta & the
presence in fetus or new born indicates
intrauterine infection.

 Relatively short lived ,disappearing earlier

than IgG

 Indicates recent infection.

 Second most abundant Ig (10% - 15%)

 Secretory Ig present in saliva, colostrum,

intestinal secretion etc.

 Relatively resistant to digestive enzymes and

reducing agents.

 Important in local immunity against respiratory

and intestinal pathogen
IgD

 Present on the surface of B lymphocyte as a

receptor and helps in antigen recognition by B
cells.
IgE
 Least mol.wt.

 Only heat labile Ig.

 Binds to basophils and mast cells and causes

release of mediators resulting in immediate
hypersensitivity reaction

 Increased in parasitic infestation & allergy

 Provides defense against most extracellular
bacterial pathogens and viruses

 Immediate hypersensitivity reactions of

Type I,II,III

 Also associated with certain auto immune

diseases
 They act mainly in two ways.

1. By direct action

2. By activation of the complement system

Direct action of antibodies

 Antibodies can inactivate invading agents in

one of the several ways.

 Agglutination

 Precipitation

 Neutralisation

 Lysis
 Direct action of antibodies are not
strong enough to play a major role in
immunity.

 Most of the protection is through the

amplifying effects of the complement
system.
 Include serum & membrane bound proteins
that function in both natural and acquired
defense system.

 These proteins are mainly enzyme precursors.

 These are highly regulated and interact via a

proteolytic cascade .
 This system is activated mainly by antigen –
antibody interaction.

 Term ‘complement’ refers to the ability of

proteins to complement or augment other
components of immune system.

 The main fractions are 9 in no. – C1 to C9.

Complement activation

 Complement is normally in an inactive form.

 When activated by antigen antibody complex,

C components react in a specific sequence as
a cascade.
 The C cascade is a series of reactions in which
the preceding components act as enzymes on
the succeeding components, cleaving them in
to dissimilar fragments.

 The larger fragments usually join the cascade.

 The smaller fragments are released.

 They possess biological effect, amplifying the

defense mechanism.
 Three different pathways activate the system.
1. The classic pathway
2. Alternative or properdin pathway
3. Mannose binding lectin pathway
 Classic pathway
 Only IgM & IgG can activate the complement
via the classical pathway.

 When an antibody binds with an antigen, a

specific reactive site on ‘constant portion’
of the antibody becomes ‘uncovered’ or
‘activated’.
 This in turn binds directly with C1 molecule of
the complement system.

 This results in a ‘cascade’ of sequential reaction,

beginning with activation of proenzyme C1.

 The C1 enzymes formed then activate successively

increasing quantities of enzymes in the later stages
of the system.

 Thus an extremely large ‘amplified’ reaction occurs.

 Multiple end products are formed & these have
important effects.

1. Opsonisation & phagocytosis

 C3b activates phagocytosis by both

neutrophils & macrophages.

 these cells engulf bacteria to which Ag – Ab

complexes are attached.

 This process is called opsonisation.

2. Lysis

 C5b6789, lytic complex has a direct effect

of rupturing the cell membranes of bacteria
or other invading organisms.

3. Agglutination

 The complement products change the

surfaces of the invading organisms.

 Thus they can adhere to one another

promoting agglutination.
4. Neutralisation of viruses

 The complement products can attack the

the structures of some viruses & render
them non virulent.
5. Chemotaxis

 C5a initiates chemotaxis of neutrophils and

macrophages.
 this causes large no. of these phagocytes
to migrate in to the site of inflammation.
6. Activation of mast cells & basophils

 C3a,C4a,C5a mediate this.

 This causes release of histamine, heparin
and several other substances.

7. Inflammatory effects

 several complement products contribute to

local inflammation.
 Alternative or properdin pathway

 It does not involve the immune complex.

 Triggered by bacterial toxins, viruses, fungi,

IgA, IgD, cobra venom, tumour cells etc.

 This does not involve C1, C2 or C4.

 Directly C3 is activated.

 C3 convertase is generated via actions of

factors B,D and properdin.
 Mannose binding lectin pathway

 This pathway is activated in the absence of

antibody.

 The rest of pathway is same as that of

classical pathway.
 They are hormone like molecules that act
generally in a paracrine fashion, to regulate
immune function.

 They are secreted by macrophages,lymphocytes

(activated T cells), endothelial cells, fibroblasts,
neurons and glial cells.
 This term includes the previously designated
lymphokines (lymphocyte derived) & monokines
(monocyte derived) that regulate immunologic,
inflammatory, and reparative host responses.

 Molecularly defined cytokines are called

interleukins.

 They mediate communication b/w leucocytes.

 Chemokines are a superfamily of cytokines that

attract WBC to areas of inflammation.
Features of some important
cytokines
1. Interleukin-1
 source - macrophages and monocytes.

 Immunological effects

 Stimulation of T cells for the production of

IL2 and other lymphokines.

B cell proliferation & antibody synthesis

 Neutrophil chemotaxis & phagocytosis

 Endogenous pyrogen

 Together with TNF, mediates hematological

changes in septic shock.
2. Interleukin - 2

 source – TH1 helper T cells.

 Activates lymphocytes, NK cells,

macrophages.
3. Interleukin - 3

 Growth factor for bone marrow stem cells.

 Stimulates multilineage hematopoiesis.

 So known as multi colony stimulating factor

(multi CSF).
4. Interleukin - 4
 source – TH2 helper T cells, mast cells,
basophils, eosinophils

 Major activator of lymphocytes & monocytes.

 Stimulates IgE production.

 So play a role in mast cell sensitization.

 Thus important in allergy & in defense

against nematode infections.

5. Interleukin - 5

 Source – TH2 helper T cells, mast cells, and

eosinophils.

 Helps in differentiation of eosinophils.

6. Interleukin - 6
 Source – TH2 helper T cells, macrophages

 Helps in activation of lymphocytes, differentiation

of B cells.

 Induces antibody synthesis by activated B cells

and formation of IL2 receptors on T cells.
7. IL- 8
 Source : T cells & macrophages.

 Helps in chemotaxis of neutrophils, basophils,

and T cells.
13. Colony stimulating factors (CSF)

 Stimulate the growth & differentiation of

pluripotent stem cells in the bone marrow.

 Eg: granulocyte (G) or mononuclear(M) CSF.

 Used to reduce neutropenia after chemotherapy
for tumours.

 Used to stimulate cell production after BM

transplantation.
1. Over reaction of system – Hypersensitivity

2. Attack against body’s own tissue –

Autoimmune diseases

3. Immune deficiency diseases -

 Excessive response to antigen

 Imbalance between the effector mechanisms

and the control mechanisms of immune
responses
 Exogenous Endogenous
antigens antigens
 Dust,pollens, foods,  Self /autologous
drugs, microbes, antigens –
chemicals – Allergy Autoimmune
disorders
 On the basis of the immunologic mechanism
that mediates the disease

1. Immediate (Type I) Hypersensitivity

2. Antibody-mediated (type II) hypersensitivity

3. Immune complex–mediated (type III)

hypersensitivity

4. Cell-mediated (type IV) hypersensitivity

 Rapid immunologic reaction

 Occurring within minutes

 Occur as a systemic disorder or as a local

reaction like skin allergy, allergic rhinitis,
bronchial asthma
 TH2 cells play a central role in immediate
hypersensitivity reactions

 It is by stimulating IgE production by B cells

and promoting inflammation

 Mast cells and basophils express a high-

affinity receptor
 It is specific for the Fc portion of IgE

 It avidly binds IgE antibodies

 When a mast cell, armed with IgE antibodies,

is exposed to the specific allergen, a series
of reactions takes place
 This leads to mast cell degranulation with
the discharge of mediators

 Results in immediate hypersensitivity

 Local type I hypersensitivity reactions have

two well-defined phases
A, The immediate or initial reaction -

 within 5 to 30 minutes after exposure to an

allergen

 vasodilatation, vascular leakage, smooth

muscle spasm or glandular secretions
B, Late-phase reaction sets in 2 to 24 hours

 Infiltration of tissues with eosinophils,

neutrophils, basophils, monocytes, and
CD4+ T cells

 Tissue destruction in the form of mucosal

epithelial cell damage
 Antibodies react with antigens present on
cell surfaces or in the extracellular matrix

 Mechanism of antibody-mediated injury

1. Opsonization of cells by antibodies and

complement components and ingestion by
phagocytes
2, Antibody-dependent cellular cytotoxicity
(ADCC)

3, When antibodies deposit in tissues, the

injury is due to inflammation
 Antigen-antibody complexes elicit
inflammation at the sites of deposition –
tissue damage

 Immune complex–mediated diseases can be

1. systemic or
2. localized to particular organs, such as the
kidney, joints
 initiated by sensitized CD4+ and CD8+ T cells

 Reactions of CD4+ T Cells: Delayed-Type

Hypersensitivity and Immune Inflammation

 Reactions of CD8+ T Cells: Cell-Mediated

Cytotoxicity
 Immune response to self antigen

 Sometimes the process that eliminate

antibodies or T cells against self antigens fail
and results in autoimmune disease.

 B cell or T cell mediated.

 Organ specific or systemic.

1, The presence of an immune reaction specific
for self-antigen

2, Reaction is not secondary to tissue damage

but is of primary pathogenic significance

3, The absence of another well-defined cause

of the disease.
A, Diseases mediated by antibodies and
immune complexes

I. Organ-specific autoimmune diseases

 Autoimmune hemolytic anemia

 Myasthenia gravis, Graves disease

II. Systemic autoimmune diseases-

 SLE (Systemic lupus erythematosus )
III. Diseases caused by autoimmunity to
microbial antigens

 Polyarteritis nodosa

B, Diseases mediated by T cells

I. Organ-specific autoimmune diseases

 Type 1 diabetes mellitus

II. Systemic autoimmune diseases

 Rheumatoid arthritis
 Systemic sclerosis

III. Diseases caused by autoimmunity to

microbial antigens

 Inflammatory bowel disease

 Immunological tolerance is the phenomenon
of unresponsiveness to an antigen as a
result of exposure of lymphocytes to that
antigen

 Self-tolerance refers to lack of

responsiveness to an individual's own
antigens
 Autoimmunity results from the
loss of self-tolerance

CENTRAL PERIPHERAL
1. Forbidden clones:

 Clonal selection theory

 Lymphocytes against self antigens get

depleted : forbidden clones

 Persistence of these clones / their

development in later life due to mutation
leads to autoimmunity
2. Hidden or sequestered antigen

 Not exposed to immune system during fetal

life.

 So no immunological tolerance against such

antigens

 Eg : lens protein, sperm antigens.

 No immunological tolerance develops against
these antigens.

 Leakage of these proteins into circulation,

evokes immune response.

 This causes damage to these proteins.

3. Neoantigen or altered antigen :

 Irradiation,drugs, sunlight – alterations in

cells of body

4. Mutations

 Immune system becomes competent for

self antigen by mutations
5. Molecular mimicry –

 Antibodies against the invading organism

cross react with normal body constituents.
 Eg: Rheumatic fever following streptococcal
infection.

 A portion of cardiac myosin resembles a

portion of streptococcal M protein.

 Thus antibodies cross react & damage the

heart
6. Unbalanced activity of helper T cells &
suppressor T cells

 Overactivity of
helper T cells AUTOIMMUNITY

 Underactivity of
suppressor T cells
Examples
1. Type 1 diabetes mellitus – against pancreatic
islet B cells.
2. Myasthenia gravis – against nicotinic
cholinergic receptors.

3. Multiple sclerosis – against myelin basic

protein and several other components of
myelin.

4. Antibodies against receptors and are capable

of activating receptor.

Eg: Grave’s d/s – against TSH receptor.

 Defense mechanism of the body are impaired.

 This leads to repeated microbial infection of

varying severity & even malignancy.

 Primary or secondary.
PRIMARY IMMUNODEFICIENCY DISEASES
 Abnormalities in the development of the
immune mechanisms.

A. Humoral immune deficiencies ( B cell defects)

 X – linked agammaglobulinemia

B. Cellular immune deficiencies (T cell defects)

 Thymic hypoplasia ( Digeorge’s syndrome)
C. Combined immunodefiencies
 Ataxia telangiectasia

D. Disorders of complement system

 Complement component deficiencies
 Complement inhibitor deficiencies

E. Disorders of phagocytosis
 Myeloperoxidase deficiency
SECONDARY IMMUNE DEFICIENCY

 Due to disease, drugs, nutritional

inadequacies, and other processes that
interfere with immune system functioning.

 More common than primary.

 Eg: AIDS
AIDS ( Acquired Immune Deficiency Syndrome)

 Agent – Human Immunodeficiency Virus(HIV)

 Transmission

 Hetero sexual & homo sexual contact.

 Contaminated blood & blood products.
 Contaminated needles.
 Mother to child transmission.
 Infected individual may be symptomless at
first & develop d/s after months or years.

 Major defect – failure of helper T cells.

 Decrease in no. of helper T cells, decreased

response to antigen, dereased production of
interleukins defective CMI

 This leads to abnormal B cell function

defective humoral immunity
 Abnormalities in macrophage & dendritic cell
function with defective antigen presentation
and cytokine secretion.

 Defect in phagocytosis defect in innate

immunity