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1. ADAPTIVE IMMUNITY
BY: DR SADAF MOEEZ

2. Acquired immunity
 Acquired immunity is immunity you develop over your
lifetime. It can come from:
1. a vaccine
2. exposure to an infection or disease
3. another person’s antibodies (infection-fighting
immune cells)
What are the 4 phases of the immune response?
• The adaptive immune response in B cells, Helper T
cells and Cytotoxic T cells involved four
phases: encounter, activation, attack, and memory.

4. FACTORS REQUIRED FOR ACQUIRED IMMUNITY

5. Major Characteristics of the Adaptive
Immune Response
 Specificity: is the ability to discriminate among different molecular entities
and to respond only to those uniquely required.
 Adaptiveness: is the ability to respond to previously unseen molecules that
may in fact never have naturally existed before on earth.
 Discrimination between self and non-self: This distinction, and the
recognition of antigen, is conferred by specialized cells (lymphocytes) that
bear on their surface antigen-specific receptors.
 Memory: a property shared with the nervous system, is the ability to recall
previous contact with a foreign molecule and respond to it in a learned
manner, that is with a more rapid and larger response(secondary response).
– Another term often used to describe immunologic memory
is anamnestic response.
• rapid production of an antibody on the second (or subsequent)
encounter with the same antigen.

10. Types of T Cells
EFFECTOR T CELLS TYPES
1. T HELPER CELLS OR TH CELLS has CD4 surface co-receptor
2. CYTOTOXIC T CELLS has CD8 surface co-receptor
The T cells differentiates in to 2 types of cells

11.  TH /T helper cells (CD4+): have a co-receptor called CD4 on their cell
surface.
 Interacts with MHC class II molecules, This allows helper T cells to
recognize pathogen peptides that have been displayed by antigen presenting
cells.
 When helper T cells recognize a peptide on an antigen presenting cell,
they become activated and begin to produce molecules called cytokines that
signal to other immune cells.
 These cells secrete cytokines which stimulate cell division of B cells and
its maturation into plasma and memory cells that eventually release
antibodies.
 Activation of macrophages to bring the process of phagocytosis.
 They also help activate cytotoxic T cells to kill infected target cells.
T-HELPER CELLS

13. TYPES OF T-HELPER CELLS

14. T follicular helper cells (Tfh) are a specialized subset of CD4+ T cells that were first
identified in the human tonsil.
They play a critical role in protective immunity helping B cells produce antibody
against foreign pathogens.
Tfh are located in secondary lymphoid organs (SLOs), including the tonsil, spleen
and lymph nodes.

15.  T helper cell lineage development and function. The cytokines
produced by dendritic cells regulate the T helper cell lineage (Th1,
Th2, Th17, T regulatory [Treg], and follicular helper T cells
[Tfh]).
 Each of them exhibits a unique phenotype, cytokine, and
transcriptional profile and exerts different functions in immune
response.
 BCL-6, B cell lymphoma 6 protein;
 CCR, C-C chemokine receptor;
 CXCR, CXC chemokine receptor;
 Foxp3, forkhead box P3;
 RORs, retinoid-acid receptor related orphan receptors;
 STAT, signal transducer and activator of transcription;
 TGF-b, transforming growth factor-beta;
 TNF, tumor necrosis factor

17. T-memory cells: The population of these cells increases only after their initial
exposure to an antigen.
If the same antigen presents itself again, they are triggered to convert
themselves into cytotoxic T cells and kill the pathogen.
TYPES OF EFFECTOR CELLS
T-suppressor cells/Treg/Regulatory T cells: have CD4 on their surface, but
they do not activate the immune system like helper T cells do
These form the part of the self-check built-in mechanism inside the body to
prevent excessive immune reactions by shutting down T cell-mediated
immunity once the pathogen has been defeated
Regulatory T cells suppress the immune response in several ways, including:
1. Producing anti-inflammatory cytokines that suppress the immune response
2. Releasing molecules that kill activated immune cells.

18. Tc (T- killer/cytotoxic) cells (CD8+):These cells interact MHC
class I molecules.
 These cells trigger the destruction of the pathogen‟s DNA by
secreting cytotoxin or creating holes in the pathogen‟s cell
membrane by perforin and granzyme.
This results in cell lysis or apoptosis.
 Cytotoxins are the chemical weapons that Killer T-cells use to
destroy infected cells.
TYPES OF EFFECTOR CELLS

20. Tc (T- killer/cytotoxic) cells (CD8+):
• Naïve CD8+ cells are also called cytotoxic lymphocyte
precursor, or CTL-P cells.
• After a CTL-P binds an antigen, it will be activated.
This will cause it to express IL-2 receptor.
• Parallelly to this activation, a Th1 cell has been
activated by an APC, which will cause the Th1 to start
secreting IL-2.
• The binding of these IL-2 to the IL-2 receptor on the
activated CTL-P cell will cause it to differentiate into
the mature cytotoxic lymphocyte, or CTL cell.

22. Effector mechanisms of CTL cells
• After a CD8+ has been activated to become a CTL
cell, it can start killing target cells.
• When the CTL binds to an infected cell or a tumor
cell it will form tight adhesions with the target
cell with the use of adhesion molecules like
integrins, creating a so-called conjugate.
• This causes the granules in the CTL to rearrange
to the side of the CTL that faces the target cell.
• The CTL will then degranulate, releasing their
granules onto the target cell by exocytosis.

23. Effector mechanisms of CTL cells
• The granules contain molecules like perforin and granzymes.
1. Perforin is an enzyme that creates a pore in the membrane of
the target cell.
2. Granzymes will then enter the target cell and kill it in two
different ways.
 Granzyme A will cause DNA-damage by a different pathway, which
will also induce the death of the cell.
 Granzyme B will activate a protein cascade called the caspase
cascade (which begins with a protein called caspase 8). Caspase 8
will activate an enzyme called CAD (caspase activated
deoxyribonuclease), which cleaves DNA eventually kills the cell.

25. Cell-mediated immune response
• This immune response is driven by T lymphocytes, Antigen
Presenting Cells such as macrophages, B cells, and dendritic
cells, and various cytokines.
• It does not use antibodies.
• Cell-mediated immunity describes a pathway that
targets endogenous antigens.
• Involve the destruction of infected cells by cytotoxic T cells,
or the destruction of intracellular pathogens by macrophages
• It mostly kills viruses and cancerous cells

26. Cancerous and virus-infected cells involve the body’s own cells and thus are not
recognized as foreign, evading normal detection
These cells may instead present antigenic fragments as a complex with their own self
markers (MHC class I)
When helper T cells identify these cells, they stimulate a second type of T lymphocyte
– cytotoxic T cells (TC cells)
Cytotoxic T cells show specificity to particular antigens and will bind to the presented
antigen and release perforating enzymes. enzymes cause the infected / cancerous cell to
by lysed, preventing the further spread of infection
Virus infected cells can also be destroyed non-specifically by NK cells, which respond
to interferon released by the infected cell