Immunity ( Medical ) - Dr Rohit Bhaskar

IMMUNITY
©2021 Dr Rohit Bhaskar PT https://www.pt-pedia.com

PRESENTED BY

OBJECTIVE
■ At the end you shoud know
■ Architecture of immune system
■ Immunity
■ Antigens
■ Antibodies
■ Immune response development
■ Other immune mechanims

ARCHITECTURE OF IMMUNE
SYSTEM
■Mononuclear Phagocytic system – also called
as Tissue Macrophage system (1960)
previously called Reticulo endothelial sytem.
■Lymphoid components – consists of network
of lymphoid organs, nodes & cells.

MONONUCLEAR
PHAGOCYTIC SYSTEM
Formation
-Monocytes from bone marrow
circulates for 3 days & then enters
tissue & becomes tissue Macrophages.

TISSUE MACROPHAGES
■
■
■
■
■
■
■
LIVER – Kupffer cells
Spleen
Bone marrow- Littoral cells
Lungs – Pulmonary alveolar
macrophages
Connective tissue –
histiocytes
Bones – osteoclasts
CNS – Microglial cells.

MONONUCLEAR
PHAGOCYTIC SYSTEM
❖Constituent cells
❖Precursor cells of
monocytes
❖Promonocytes
❖monocytes

MONONUCLEAR PHAGOCYTIC
SYSTEM
Functions
1 Role in inflammation & healing
2 Role in defence against bacteria
3 Role in immune response
4 Role in removal of old RBC
5 Role in removal of old WBC & platelets
6 Storage function.
Saturday, June 16, 2018

LYMPHOID COMPONENTS
Primary lymphoid tissue
■ Thymus – contains Thymocytes containing
thymocin.
▪ Role – education of lymphocytes to become T
lymphocytes.
▪ Effects of thymectomy – marked infection.

LYMPHOID COMPONENTS
Primary lymphoid tissue
■ Bursa equivalent – bone marrow
■ Lymphocyes from bone marrow become B
Lymphocytes
■ Form plasma cells & antibodies.

PERIPHERAL
LYMPHOID ORGANS

PHAGOCYTOSIS

PHAGOCYTOSIS
■ Stages
■ Margination
■ Diapedesis
■ Chemotaxis
■ Peudopodia formation – engulfment
■ Killing / degradation

ANTIGEN
■ Definition
■ Hapten
■ Immunogenicity
■ Antigen specificity
■ Species specificity
■ Isospecificity

HISTOCOMPATABILITY ANTIGENS
■ Major Histocompatability complex
(Chromosome 6-short arm)
■ MHC Class I
■ MHC Class II
■ MHC Class III

CELL MEDIATED IMMUNITY
■ Role of cellular immunity
■ Intracellular bacteria– M.tuberculosis, M.leprae
■ Viruses
■ fungi
■ Allograft rejection & graft versus host
reaction
■ Delayed hypersensitivity & autoimmune

TYPES OF IMMUNE RESPONSE
■ Primary
■ Secondary

STAGES
■ Antigen processing and presentation

RECOGNITION OF
ANTIGEN BY
LYMPHOCYTES

T-LYMPHOCYTES
DIFFERENTIATION (ACTIVATION)
CD8 types
CD4 types
TT co-operation
Memory cells

ATTACK PHASE
■ Role of cytotoxic T- cell
■ Lysis through cytotoxic substances
■ Induction of Apoptois
■ Perforin mediated killing

HELPER T CELL

MEMORY CELLS

HUMORAL MEDIATED IMMUNITY
■ Role of humoral immunity
■Extracellular bacterial pathogens.
■Immediate hypersensitivity
■Autoimmune diseases.

STAGES
•Recognition of antigens by lymphocytes
■ Lymphocyte activation
■ Activation of T-lymphocytes.
■ Activation of B-lymphocytes.
■ Antigen processing and presentation
■
■ Role of plasma cells
Role of memory cells

■ PRODUCTION
OF ANTIBODIES
■ Theories of antibody
production
■ Clonal selection theory
(Burne 1957)
■ Inactivation or attack
phase
■ Direct attack
■ Complement system

DIRECT ATTACK

COMPLEMENT SYSTEM
■ Classical pathway.
■ L - Lysis
■ A - Agglutination
■ N - Neutralization
■ A – activation &
degranulation of
mast cells
■ C - chemotaxis
■ O- Opsoniozation.
■ Alternate pathway.

COMPLEMENT SYSTEM

ANTIBODIES
■ Structure
■ Heavy Chain
■ Light Chain

TYPES
■ Immunoglobulins (Ig)
■ Ig G
■ Ig A
■ Ig M
■ Ig D
■ Ig E

IMMUNOGLOBULINS
FEATURE IgG IgA IgM IgD IgE
H chain γ α μ δ ε
L chain Κ or λ Κ or λ Κ or λ Κ or λ Κ or λ
Mol wt
(kd)
150 160-385 900 180 190
Serum
conc
12 2 1.2 0.03 0.00004
Half life 21 6 5 3 2
Placental
T
Yes No No No No
Compleme
nt fixation
C A C N N
ROLE Body
fluids
Body
surface
Blood
stream
Not known Type 1
hypersens
itivity

OTHER IMMUNE MECHANISM
RELATED ASPECTS.
■ Immune tolerance
■ Immune modulation
■ Autoimmunity
■ Hypersensitivity
■ Immunodeficiency diseases.

IMMUNE TOLERANCE
■ Def – State of
unresponsiveness to
an antigen.
■ Types.
■ Natural – Non-
responsiveness to self
antigen.

IMMUNE TOLERANCE
■ Acquired.
■ General – Due to
impairment of
immune system.
■ Specific – specific
antigen becomes
tolerogenic.

MECHANISM OF TOLERANCE
■ Clonal deletion – clones
are selectively deleted.
■ Clonal synergy – cones of
cells might remain but not
activated.
■ Clonal Suppression –
Inhibited through active
suppression.

FACTORS INFLUENCING
INDUCTION OF TOLERANCE.
■ Species –tolerance varies from species to species
■ Immunological competency of the host.
■ Antigen – Physical nature, Dose, Route of
administration.
■ Age of the host.

TOLERANCE TO FOETUS.
■Factors
■Placenta
■Alpha fetoproteins –
immunosuppressive agents
■Progesterone
■Fetal T cells.

IMMUNE MODULATION
■ Immune Enhancement – increase in response
in terms of Rate, Intensity, Duration
■ Adjuvant – Non-specifically enhance immune
response to an antigen.

IMMUNE ENHANCEMENT
■ Mechanism of action
■ Alter distribution & persistence of antigens
■ Stimulate lymphocyte number.
■ Activate Macrophages.
■ Types
■ Incomplete
■ Complete

IMMUNE SUPPRESSION
■ Immune suppression – Reduction in
immunological response.
■ Specific
■ Non-specific.
■ Immunosuppressive agents.
■ Physical
■ Chemical
■ Biological.

PHYSICAL
■Irradiation
■Surgical
procedures.
■Thymectomy
■Splenectomy
■Thoracic duct
drainage.

CHEMICAL
■ Corticosteroids.
■ Impair maturation of activated cells
■ Suppress production of antibodies
■ Cyclosporins – Inhibit IL-2
■ Cytotoxic drugs – Inhibit nucleic acid synthesis &
replication.

BIOLOGICAL
■ Antigen induced suppression – Desensitization
against allergen
■ Antibody induced suppression – used in
pregnant mothers.
■ Anti-lymphocytic serum.

AUTOIMMUNITY
■ Mechanism
■ Forbidden clones.
■ Hidden antigen or
sequestrated antigens
■ Neo antigens or altered
antigens
■ Cross reacting antigens
– molecular mimicry
■ Mutations
■ Unbalanced activity of
Helper & suppressor T
cells.

AUTOIMMUNE DIEASES.
■ Autoimmune anemia
■ Thrombocytopenic purpura.
■ Grave’s disease
■ Hashimoto’s disease
■ Insulin dependent diabetes mellitus.
■ Rheumatoid arthritis.
■ Rheumatic fever.

HYPERSENSITIVITY
Abnormal response which produces
physiological or histopathological
damage in the host

HYPERSENSITIVITY
■ Type I – local
Anaphylaxis
■ Systemic &
generalized
anaphylaxis.
■ Mechanism –
Degranulation of mast
cells & basophils by
Ag-Ab complex.
■ Type II – Immediate
reaction
■ Examples –
Incompatible blood
transfusion,
Autoimmune
hemolytic anaemia,
Hemolytic disease of
newborn.

HYPERSENSITIVITY
■ Type III (Immune
complex mediated) –
damage of the
complex deposited in
tissue.
■ Type IV – Delayed.
■ Tuberculin tests
■ Contact dermatitis

IMMUNODEFICIENCY DISEASES
■ Defect may be in the
■ Lymphocyte & Natural killer cells
■ Phagocytic cells
■ Complement proteins.
■ PRIMARY Immunodeficiency
■ SECONDARY.

PRIMARY IMMUNODEFICIENCY DISEASE
■ Humoral immune deficiency
■ Cellular immunodeficiency.
■ Combined
■ Complement immunodeficiency.
■ Phagocytic disorders.

SECONDARY
IMMUNODEFICIENCY DISEASE.
■ AIDS – Acquired immunodeficiency syndrome.
■ Reduction in Helper T cells
■ First detected in USA 1981 (India-1986)
■ Spread of disease – sex workers, drug addicts,
homosexual males & unscreened blood transfusion.

AIDS – ACQUIRED
IMMUNODEFICIENCY SYNDROME.
■ Transmission – 3 routes
■ Parenteral
■ Sexual
■ Transplacental.
■ Structure of HIV –
Retrovirus.
■ Core – 2 single strands of
genomic RNA, enzyme
reverse transcriptase &
protein P-15

AIDS – ACQUIRED
■ Virus Multiplication
– virus comes in
contact with T4
antigen – passes into
cell – genomic RNA
synthesizes copy DNA
with help of reverse
transcriptase.

AIDS – ACQUIRED
■ Incubation period – 2-10
years
■ Window period – 2-6
months (tests are negative)
■ HIV positivity indicated by
■ Presence of P24
■ Antiviral antibodies
■ Reduced T cells

AIDS – ACQUIRED
■ Signs & symptoms –
mostly opportunistic
infections due to low
immunity
■ HIV tests.
■ screening tests - ELISA
■ Supplement tests –
Wesrnblot essay
■ Confirmatory tests – virus
isolation, p24 detection

AIDS – ACQUIRED
■ Prevention
■ Education
■ Screening
■ Ban on prostitution.
■ Safer sex
■ Use of disposable
instruments.
■ Treatment – Triple drug treatment.
■ Protease inhibitor,
■ Reverse transcriptase inhibitor,
■ Azidothymidines
■ Interleukins

OBJECTIVES
■ At the end you shoud know
■ Architecture of immune system
■ Immunity
■ Antigens
■ Antibodies
■ Immune response development
■ Other immune mechanims

Immunity ( Medical ) - Dr Rohit Bhaskar

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