The adaptive immune response involves B cells, T cells, cytokines, and antibodies working together in a complex network. It matures over a person's lifetime and provides stronger and more effective protection compared to the innate immune response. The adaptive response includes both humoral immunity, which is antibody-mediated and defends against extracellular pathogens, and cell-mediated immunity, which does not involve antibodies.
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Adaptive Immune Response Overview
1. IMMUNE RESPONSE
Immune response = collective and coordinated
response to the introduction of foreign substances
in an individual mediated by the cells, tissues,
organs and molecules of the immune system
2. Immune Response
Review: Innate response - non-specific, limited
in its response (cannot handle too much
invasion)
Adaptive Immune response
– Matures over person’s lifetime
– Takes time to start up
– More effective and very powerful
– Important Hallmark : MEMORY
– Complex, involves a network of cells: cytokines, B
cells, T cells, antibodies
4. Humoral Immunity - Applications
Defense against
most extracellular bacterial pathogens
viruses that infect through the respiratory or intestinal
tracts
Prevents recurrence of viral infections.
We see antibody production
Takes part in the pathogenesis of Immediate
(Types 1, 2 & 3) hypersensitivity & certain
autoimmune disorders.
5. Humoral Immunity
Cells taking part in immune response
- Antigen presenting cells (APCs)
- B cells &
- T cells
Production of antibodies consist of following
stages :
1. Ag capture & processing by APCs
2. Ag presentation
3. TH cell activation
4. B cell stimulation & differentiation
5. Ab production by plasma cells
6. 1. Antigen Capture & Processing
Captured by APCs (macrophages & dendritic
cells) – broken down in to small peptides.
2 different pathways for Ag processing
depending on their origin
Exogenous Ag – Endocytic (class II) pathway within
lysosomes
OR
Endogenous Ag – Cytosolic (class I) pathway in the
Endoplasmic reticulum.
7. 2. Antigen Presentation
Peptides derived from
1. Exogenous Ags – presented with MHC class
II molecule, recognised by TH cells.
2. Endogeous Ags – presented with MHC class
I molecule, recognised by TC cells.
9. 3. Helper T cell Activation
Activation requires 2 signals:
1. Combination of TCR with the Ag peptide-MHC class II
complex.
2. Co-stimulatory signal : combination of B7 on APC &
CD28 on the T cell with release of IL-1 .
Activated TH cells now produce IL-2 which
supports the growth of itself & other T cells.
Also produce IL-4, IL-5 & IL-6 which stimulates
the growth & differentiation of B cells into
- Plasma cells & Memory B cells
13. 5. Ab production
Ab production follows a characteristic
pattern consisting of :
1. Lag Phase – immediate stage following
antigenic stimulus during which Ab is not
detectable in the circulation.
2. Log Phase – steady rise in the titre of Abs.
3. Plateau or Steady Phase – equilibrium
between Ab synthesis & its catabolism.
4. Decline Phase – catabolism exceeds
production, fall in Ab titre.
14.
15. Primary & Secondary Response
Primary Response
Initial contact with
the Ag
Slow, sluggish & short
lived.
Long lag phase.
Low titres of Ab, does
not persist for long.
IgM – predominant.
Secondary Response
Response to
subsequent exposure
to the same Ag.
Prompt, powerful &
prolonged.
Short or negligible lag
phase.
Very high levels of Ab,
lasts for long periods.
IgG - predominant
16. Phases
1. A single injection of an Ag helps in
sensitising / priming the immunocompetent
cells producing the particular Ab.
2. Subsequent injections of an Ag – Boosters –
induce effective levels of Ab.
Hence multiple doses of non living vaccines
are administered to achieve effective levels
of immunity.
17. Phases
With live vaccines, a single dose is sufficient
as multiplication of the organism will provide a
continuous stimulus.
“Negative Phase” – when an Ag is injected
into an animal already carrying the specific Ab
in circulation, a temporary fall in the level of
Ab occurs due to the combination of Ag with
the Ab. It is then followed by a rise in Ab titre.
18. Cell Mediated Immunity
Refers to the specific immune responses that
do not involve antibodies.
CMI response 1st described by Jenner in
1798.
1890 - Koch described the exaggerated
cutaneous reaction of tuberculous guinea
pigs to the I.D. injection of tubercle bacillus –
Delayed hypersensitivity (DH).
DH- skin lesions appear 48-72 hrs after
administration of the Ag.
19. Applications of CMI
CMI participates in following immunological
functions :
1. Delayed hypersensitivity.
2. Immunity in infectious diseases caused by
obligate & facultative intracellular parasites
Bacteria – Mycobacteria, Listeria
Fungi – Histoplasma, Blastomycetes
Protozoa – Leishmania,Trypanosoma
Viruses – Measles, Mumps
20. Applications of CMI
3. Transplantation immunity & graft-versus-
host reaction.
4. Immunological surveillance & immunity
against cancer.
5. Pathogenesis of certain autoimmune
diseases
e.g. Thyroiditis
21. Cells involved in CMI
CD8+T cells - recognise antigenic peptides in
association with MHC class I molecule on a
target cell.
CD4+T cells - MHC class II restricted, secrete
cytokines which help in the growth &
differentiation of T lymphocytes.
22.
23.
24.
25. Scheme of Immune
response
against T cell
dependent Ags
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26. Factors influencing Ab production
1. Genetic factors
2. Age
3. Nutritional status
4. Route of administration of Ag & site of injection
5. Size & number of doses
6. Multiple Ags
7. Adjuvants
8. Immunosuppressive agents
9. Effect of antibody
27. CYTOKINES
Biologically active substances (intercellular
messengers) which are
– produced transiently
- exert their effects at very low (10–15) conc. &
- regulate immunological, inflammatory &
reparative host responses.
Includes – Interleukin (product of leucocytes)
- Interferons
- Growth factors & others
28. Features of Cytokines
Mediate their actions by binding to specific cell-
surface receptors.
Produced by wide variety of cells like lymphocytes,
macrophages, platelets & fibroblasts.
Cytokines can have
1. Paracrine effect – act locally near the producing
cells
2. Autocrine effect – act directly on the producing
cells
3. Pleiotropic effect – multiple effects on growth &
differentiation of various cell types.
29. Cytokines: Source & Function
Cytokines
IL-1
IL-2 T cells Proliferation and/or activation of T
& B cells
IL-4 T & B cells, mast cells, Activation of B cells, differentiation
of Th2 cells
IL-6 T cells, macrophages Differentiation of T & B cells
IL-10 T & B cells, macrophages Suppression of macrophages,
activation of B cells
IL-12 B cells, macrophages Differentiation of Th1 cells
IFN Leucocytes Antiviral activity
IFN Fibroblasts
IFN T cells
Source : Immune cells Effects of Cytokines
Monocytes, macrophages Activation of T & B cells