The document discusses adaptive immunity and the immune response. It describes the four phases of the adaptive immune response as encounter, activation, attack, and memory. Acquired immunity develops over one's lifetime from vaccines, infections, or antibodies from others. The adaptive immune response involves B cells, helper T cells and cytotoxic T cells. It also discusses the specificity, adaptiveness, discrimination between self and non-self, and memory properties of the adaptive immune response. The major cell types involved are T helper cells, cytotoxic T cells, T memory cells, and regulatory T cells. The roles and mechanisms of these cell types are described in detail.

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