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Hema Presentation-Grp 6

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11 views44 pages

Hema Presentation-Grp 6

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drabdullah843
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GROUP 6

Member Roll no #
s
Malaika 44
Rukhsana 45
Gulzar 46
M.Ihtisham 48
Absar 49
Haiqa Mushtaq 50
Danish Nawaz 51
Zoha Javed 52
Rena Gull
Muhammad
Adeel
THE WHITE CELLS 2
:
Lymphocytes and their benign
disorders
LYMPHOCYTES
NATURAL KILLER
CELLS

BY
RUKHSANA
GULZAR
LYMPHOCYTES

A lymphocyte is a type of white blood cell that is part of the immune system.

They are the immunologically competent cells that assist phagocytes in defense
of the body against infection and other foreign invasion.

In postnatal life , primary lymphoid organs are those in which lymphocytes are
produced and matured. These are bone marrow and thymus.

Secondary lymphoid organs are where mature lymphocytes interact with


antigens and are activated to mount an immune response. These are
lymph nodes and spleen.
Types of lymphocyte: TYPES
1.B Lymphocyte
2.T Lymphocyte

B CELL & T
CELL
B LYMPHOCYTES

Origin : Produced and matured in bone marrow

Primary function : Produce antibodies and role in humoral immune


response

Activation : Activated when they encounter a specific


antigen that their receptor
Upon activation , they differentiate into
plasma cells (produce antibodies)
or memory B cells(provide long-term immunity by
remembering
past infections)

Surface Markers : Express surface proteins such as


CD19 , CD20
B- Cell receptors (BCR)
T LYMPHOCYTES

Origin : Produced in bone marrow and matured in thymus

Primary function : Central to cell mediated immunity


Directly attack infected or cancerous cells

Activation : Activated by recognizing specific antigens presented by APCs via MHC molecules

Surface Markers : Express specific surface proteins like CD3 , CD4 (helper T cells) or CD8 (cytotoxi

Types of T cells : Helper T Cells (CD4+)


Cytotoxic T Cells (CD8+)
Regulatory T Cells
T Cell Activation Types of T Cell
NATURAL KILLER CELLS

are a type of lymphocyte in the innate immune system that plays a key role in the body’s first line of defen
st infections and tumors.

lls kill target cells by releasing cytotoxic molecules , such as perforin and granzymes , which induce apopto
ed cells.

can respond rapidly to infected or cancerous cells without needing prior exposure to the pathogen.

do not rely on antigen recognition through specific receptors like B and T cells but instead recognize stresse
through a balance of activating and inhibitory signals

interact with other immune cells by producing cytokines that help shape the adaptive immune response.
also interact with dendritic cells to influence the direction of immune responses.
NK CELLS

Origin : Originate in bone marrow


Part of innate immune system

Primary function : Recognize and kill virally infected cells without prior sensitization
Do not require antigen presentation or recognition of MHC molecules , unlike T cells

Mechanism of Action : Use two main methods to induce cell death


Release of cytotoxic granules
Antibody-Dependent Cellular Cytotoxicity (ADCC)

Receptors : Activating and inhibitory receptors that regulate their activity


Killer Immunoglobulin-like Receptors (KIRS)
Natural Cytotoxicity Receptors (NCRS)
Natural
Killer
Cell
IMMUNOGLOBILINS

BY
DANISH NAWAZ
IMMUNOGLOBILINS

mmunoglobulins are also called antibodies.


Antibodies are proteins that your immune system makes to fight germs, such as viruses and bacteria.
Each antibody is specific to a particular antigen.

STRUCTURE OF IMMUNOGLOBULINS

globulins are Y-shaped proteins produced by B cells in response to the presence of antigens in the body.

structure consists of:


eavy chains (H chains):
These are long chains that form the stem of the Y shape.
ght chains (L chains):
These are shorter chains that form the arms of the Y shape.
ble regions (Fab):
These are the tips of the Y shape, responsible for recognizing and
binding to specific antigens.
ant regions (Fc):
These are the stem and base of the Y shape, responsible for interacting
er immune cells and triggering immune responses.
BINDING SITES OF ANTIGENS
ON ANTIBODY

Binding sites of antigen on antibody are


gA...2
gD...2
gE...2
gG...2
gM...10

The heavy and light chains are held together by disulfide bonds,
and the variable regions are highly variable in their amino acid sequence.
CLASSES

ive main classes of immunoglobulins

gG:
The most abundant type, it provides long-term protection by
recognizing and neutralizing pathogens.

gA:
Found mainly in mucosal areas such as the gut, respiratory tract,
nd urogenital tract, as well as in saliva, tears, and breast milk.

gM:
The first antibody produced in response to an infection.

gE:
Involved in allergic reactions and protection against parasitic infections.

gD:
Present in small amounts in the blood and mainly found on the surface
of immature B-lymphocytes.
ANTIGEN-RECEPTOR GENE
REARRANGEMENT

BY
IHTISHAM ABSAR
ANTIGEN-RECEPTOR GENE REARRANGEMENT

Antigen receptor gene rearrangement is a process that occurs in immune cells


(B cells and T cells) to generate diverse receptors that recognize antigens".
B Cell Receptor (BCR) Rearrangement:

1.V (Variable), D (Diversity), and J (Joining) gene segments:


The BCR locus contains multiple V, D, and J gene segments.
2. Rearrangement:
Enzymes (RAG1 and RAG2) catalyze the rearrangement of V, D, and J segments
to form a unique VDJ combination.
3. V(D)J recombination:
The V, D, and J segments are joined through a process called V(D)J recombination,
forming a functional BCR gene.
4. Immunoglobulin (Ig) heavy chain:
The rearranged VDJ segments encode the Ig heavy chain.
5. Light chain rearrangement:
A similar process occurs for the Ig light chain, using V and J segments.
6. BCR assembly:
The heavy and light chains combine to form a functional BCR.
T Cell Receptor (TCR) Rearrangement:

1. V, D, J, and C (Constant) gene segments:


The TCR locus contains multiple V, D, J, and C gene segments.

2. Rearrangement:
Similar to BCR, RAG1 and RAG2 catalyze V, D, and J
segment rearrangement.

3. V(D)J recombination:
V, D, and J segments are joined to form a functional TCR gene.

4. TCR α and β chains:


Rearranged VDJ segments encode the TCR α and β chains.

5. TCR assembly:
The α and β chains combine to form a functional TCR.
IMPORTANCE

1.Specificity:
Each immune cell expresses a single, unique receptor, ensuring specific recognition and
response to antigens.

2. Adaptability:
Rearrangement enables the immune system to adapt to new pathogens and mutations.

3. Immune tolerance:
Rearrangement helps eliminate self-reactive immune cells, preventing autoimmune diseases.

4. Immune response:
Rearrangement enables the activation of immune cells and generation of memory cells,
providing long-term immunity, and collectively leading to an effective immune response.

5. Pathogen clearance:
Rearrangement helps eliminate pathogens by generating receptors that recognize and
bind to specific antigens.
DISEASES ASSOCIATED WITH ANTIGEN-RECEPTOR GENE
REARRANGEMENT’S MALIGNANCIES

1.Immunodeficiency:
Inability to produce functional antigen receptors, leading to impaired immune responses.

2. Autoimmunity:
Production of self-reactive antigen receptors, leading to autoimmune diseases like Rheumatoid Arthritis.

3. Cancer:
Uncontrolled proliferation of immune cells with mis rearranged antigen receptors,
leading to lymphoproliferative disorders like leukemia or lymphoma.

4. Allergic Reactions:
Overactive or misdirected immune responses lead to chronic inflammation and allergic reactions.

5. Immune dysregulation:
Disrupted and impaired balance of immune responses, leading to immune-related disorders.
THE COMPLEMENT
SYSTEM

BY
MUHAMMAD
ADEEL
THE COMPLEMENT SYSTEM

The complement system is a part of the immune system that enhance the ability of
antibodies and phagocytic cells to clear or remove pathogens from an organism.

It consists of a group of proteins that work together to help in the elimination of


pathogens, such as bacteria and viruses, from the body".

KEY COMPONENTS

1.C1-C9:
These are the nine major proteins that make up the complement system.

2. C1q, C1r, and C1s:


These proteins form the C1 complex, which initiates the classical pathway.

3. Factor D:
This protein is involved in the alternative pathway.
PATHWAYS OF COMPLEMENT ACTIVATION

1. Classical Pathway:

- Activated by antibodies bound to pathogens


such as IgG and IgM coating of cells.

- C1q binds to antibodies, activating C1r and C1s.

- C4 and C2 are cleaved, forming C4b and C2b.

- C3 convertase (C4b2b) cleaves C3, forming C3b.2.

2. Alternative Pathway:

- Activated by IgA and Endotoxin (from gram negative Bacteria).

- Factor D cleaves factor B, forming Bb.

- C3 convertase (C3bBb) cleaves C3, forming C3b.


Functions of the Complement System:

ization:
Complement proteins mark pathogens for destruction by phagocytic cells.
rane Attack Complex (MAC):
Complement proteins form a MAC, which creates a hole in the pathogen's cell membrane, leading to its
mmation:
Complement proteins promote inflammation, which helps to isolate and eliminate pathogens.
DISEASES ASSOCIATED WITH COMPLEMENT DYSREGULATION
MALIGNANCIES

1.Autoimmune disorders:
Systemic lupus erythematosus (SLE), rheumatoid arthritis (RA).
2. Inflammatory diseases:
Asthma, atopic dermatitis, Meningitis, sepsis.
3. Hematological disorders:
Paroxysmal nocturnal hemoglobinuria (PNH),
atypical hemolytic uremic syndrome (aHUS).

TREATMENT

Complement Inhibitors Immunotherapy


Monoclonal Antibodies Stem Cell Transplantation
Chemotherapy Plasma Exchange
Targeted Therapy Complement Modulators
THE IMMUNE
RESPONSE

BY
MALAIKA
THE IMMUNE RESPONSE

The immune response is a complex, multi-layered defense system that


protects the body
from harmful pathogens like bacteria, viruses, fungi, and parasites.

Specific Immune Response:

T and B cells produce highly specific responses due to unique receptors on


their surface.
Lymphocytes(T and B cells) develop in bone marrow and thymus.
Antigen-presenting cells (APCs), like dendritic cells, process and present
antigen to T and B cells.
Each lymphocyte has a distinct receptor, allowing them to recognize specific
antigens.
When an antigen binds to a B cell’s receptor, it can trigger activation
leading to ;

-Effector cells (produce antibodies)


Dendritic Cell (DC) Precursor Migration
and Antigen Capture

ndritic Cell(DC) precursors migrate from blood into tissues at low levels,
easing in response to inflammation or infection.

mature DCs in tissues are efficient at micropinocytosis,


rocess allowing them to capture antigens from their environment.

tured antigens are then processed and presented to T-Cells,


gering an immune response.
T Cell Recognition

1. Antigen presenting cells (APCs) process and present antigens on MHC molecules.

2. T cells recognize antigens through their T cell receptor (TCR).

3. CD4+ T cells recognize antigens presented on MHC II molecules.

4. CD8+ T cells recognize antigens presented on MHC I molecules.

T Cell Activation

1. TCR binding to antigen-MHC complex triggers signaling pathways.

2. Co-stimulatory signals from APCs (e.g.,CD28, CD40) enhance activation.

3. Activated T cells proliferate, differentiate, and acquire effector functions.

4. T cells can become memory T cells, providing long term immunity.


Antigen-Specific Immune Response
Generation
Antigens enter secondary lymphoid organs, triggering
immune responses.
B cells recognize antigens via surface immunoglobulins,
and most antibody responses require T cell help.

However, some antigens can stimulate T cell-


independent
B cell responses.

1.Antigen presentation in follicle centers

2. B cell activation and migration to germinal centers

3. Somatic hypermutation and selection by T cells

4. Differentiation into memory B cells or plasma cells

5. Plasma cells produce high-affinity antibodies


LYMPHOCYTOSIS

BY
ZOHA JAVED
LYMPHOCYTOSIS

hocytosis is a medical condition characterized by an elevated number of lymphocytes in the blood.

hocytosis often occur in infants and young children in response to infections that produce a
ophil reaction in adults.

CAUSES

ection
ute: infection mononucleosis, rubella, mumps,

ute infection lymphocytosis, hepatitis, HIV, Cytomegalovirus.

ronic: syphilis. It may causes by primary infection with Epstein-Barr virus (EBV).

V infection is also known as infectious mononucleosis.


CLINICAL FEATURE OF LYMPHOCYTOSIS

A prodomal period of a few days occur with


lethargy, malaise , headaches, stiff neck, and a dry
cough.
In established disease ,the following features may
be found:

1.Sore throat with inflamed oral pharyngeal


surface

2.Follicular tonsillitis 3.Fever may be mild or severe

3.Rashes

4.Splenomegaly occur in half of patients

5.Hepatomegaly in approximately 15%

6.5% of patient are jaundiced


DIAGNOSIS OF LYMPHOCYTOSIS

boratory tests:

omplete Blood Count (CBC): Measures white blood cell count, including lymphocytes.

lood Smear: Examines blood cell morphology, including lymphocytes.

ow Cytometry: Analyzes lymphocyte subsets and surface markers.

mmunophenotyping: Identifies lymphocyte surface antigens

erophile antibodies : Modern slide screening tests such as the MONOSPOT TEST ,
ormalinized horse red cells to test for the IgM antibodies which agglutinate the cells
TREATMENT OF LYMPHOCYTOSIS

1.In the great majority of patients only symptomatic treatment is required.

2.Corticosteriods are sometime given to those with severe systemic symptoms.

3.Most patients recover full 4-6 weeks after initial symptoms


IMMUNODEFECIENCY

BY
HAIQA MUSHTAQ
IMMUNODEFECIENCY

munodeficiency refers to a condition where the immune system is weakened or impaired,


king it difficult for the body to fight off infections.

munodeficiency is also frequently associated with tumors of the lymphoid system


luding chronic lymphocytic leukemia and myeloma.
CAUSES

1. Genetic disorders (e.g., HIV)


2. Infections (e.g., HIV/AIDS)
3. Medications (e.g., immunosuppressants)
4. Cancer and its treatment (e.g.,
chemotherapy)
5. Autoimmune disorders (e.g., rheumatoid
arthritis)
6. Nutritional deficiencies (e.g., vitamin D
TYPES OF IMMUNODEFECIENCY

Primary Immunodeficiency (PID): Congenital or inherited disorders.


Secondary Immunodeficiency: Acquired disorders.
Combined Immunodeficiency: Combination of PID and secondary immunodeficiency

SYMPTOMS

1. Recurring infections (e.g., pneumonia,


sinusitis)
2. Chronic diarrhea
3. Fatigue
4. Weight
5. Skin rashes
6. Autoimmune disorders
TREATMENT

1.Antibiotics and antivirals for infections

2. Immunoglobulin replacement therapy

3. Bone marrow transplantation

4. Gene therapy

5. Immune system modulators


DIFFERENTIAL DIAGNOSIS OF
LYMPHADOENOPATHY

BY
RENA GULL
DIFFERENTIAL DIAGNOSIS OF LYMPHADOENOPATHY

efinition:
Lymphadenopathy is the enlargement of lymph nodes which are
small, bean- shaped organs that are part of the immune system

TYPES

eneralized Lymphadenopathy:
Enlargement of lymph nodes in multiple locations
calized Lymphadenopathy:
Enlargement of lymph nodes in a specific location

mples of Localized Lymphadenopathy


vical lymph nodes
lary lymph nodes
uinal lymph nodes
CAUSES

Infectious causes Neoplastic causes


•Bacterial: -Lymphoma
-Tuberculosis -Leukemia (acute or chronic)
-Cat - scratch disease -Metastatic cancer (e.g., breast, lung, colon)
•Viral: Inflammatory causes
-HIV -Sarcoidosis
-EBV -Systemic lupus eethematosus (SLE)
-CMV
•Fungal: Other causes
-Histoplasmosis -Lipid storage disease (e.g Gaucher 's disease)
-Castleman disease
SYMPTOMS DIAGNOSTIC
TESTS

Swollen lymph nodes BLOOD TESTS


Complete Blood Count (CBC)
Fever Blood Chemistry
IMAGING STUDIES
Fatigue CT Scan
MRI
Ultrasound
Weight loss LYMPH NODE BIOPSY
INFECTIOUS DISEASE TESTING
Night sweats HIV
TB
THANKYOU

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