IMMUNOLOGY Flashcards

1
Q

OBJECTIVES

A

Define and contrast the terms “innate or natural” and “acquired or adaptive” immune
responses.
2. Classify the immune cells and relate their structures and components to their functions
in innate and adaptive immunity.
3. Identify the primary and secondary lymphoid organs and explain their differentiation
4. Briefly compare and contrast the structure of the thymus, lymph node, spleen and
Peyer’s patch.
5. Describe briefly with the aid of diagrams, the recirculation of lymphocytes.
6. Categorise the terms “humoral”,“cell-mediated”, “active” and “passive”immunity.
7. Describe with the aid of a simple diagram, the basic structure of the immunoglobin
molecule, identifying the antigen binding site and Fc portion of the molecule.
8. Identify the various immunoglobin classes and subclasses in humans, and relate their
individual structures to their functions.
9. Explain antigen, immunogen and antibody.
10. Outline the principles of the generation of antibody diversity.
11. Compare and contrast the following receptors: MHC, BCR and TCR, by their
structures and functions.
12. Outline the developmental pathway of the B-lymphocyte in the bone marrow and its
further differentiation after antigen stimulation.
13. Differentiate between primary and secondary antibody responses, relating the
importance of isotoype switching, affinity maturation and immunological memory
processes.
13
14. Outline the development of T-lymphocytes in the thymus and briefly describe positive
and negative selection.
15. Explain the differentiation of T lymphocytes into their various types and relate their
functional differences.
16. Illustrate the gene map of the Major Histocompatibility Complex. Draw simple
diagrams to illustrate the structure of MHC Class I and II molecules. Compare the
distribution of these molecules.
17. Outline the mechanisms for processing of antigens, the major APCs and their
locations.
18. Outline the stages of activation, proliferation and differentiation of T-lymphocytes in
response to presented antigen.
19. Describe the role of T-cells in cell-mediated cytotoxicity, macrophage activation,
delayed hypersensitivity and T-cell/B-cell co-operation.
20. Draw a simple diagram of the complement pathways. List the major functions of
complement giving examples of specific components mediating these effects.
21. Define an immune complex. Describe the role of immune complexes in antigen
clearance and the generation of inflammation. Outline the factors involved in the
removal of immune complexes.
22. Define the term “cytokine.” Describe the general properties of these molecules. List
the major cytokines involved in the acute phase response regulation of
haematopoiesis, phagocyte function and T-cell, B-cell and NK cell function.

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2
Q

HOW DOES INFECTION GET IN

A

INFECTION GETS IN BY PHYSICAL BARRIER: SKIN, PH ,CILIA
MOLECULAR BARRIER: COMPLEMENT, INTERFERON

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3
Q

PHYSICAL BARRIERS TO INFCETION

A

ADD IN PHOTO

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4
Q

WHAT ARE THE FORMATION OF LEUCOCYTES

A

PHOTO

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5
Q

HAEMATOPIOEIS CELLULAR DIFFERENTCIATION

A

PHOTO

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6
Q

MULTIPOTENTIAL HAEMATOPOIETIC STEM CELL

A

Responsible for blood and immune cells (white blood cells)
1)Multipotent
2) Ability to differentiate into all functional blood cells
3) Self-renewal
4) Ability to give rise to HSC without differentiation

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7
Q

COMMOM LYMPHOID PROGENITOR (CLP)

A

1-Earliest lymphoid progenitor cell
2-Gives rise to T, B and NK cells along with DCs

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8
Q

B LYMPHOCYTE- B CELL

A

1- Named ‘B’ cell due to its location
2-Produces antigen specific immunoglobulins, aka, antibodies, against invasive pathogens.
3- Also presents antigens and secrete cytokines.

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9
Q

T LYMPHOCYTE- T CELL

A

1- 2 LYMPHOCYTE CELL NAMED ‘T’ DUE TO ITS LOCATION OF MATURATION ( THYMUS GALND)
2-Various types exists with varying functions
3-Responsibilities include assisting B cells, production of cytokines, regulation of immune responses and killing of infected and cancerous cells

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10
Q

NATURAL KILLER CELLS NK CELL

A

1- Functions include
Killing of virally infected cells
Detecting and controlling early signs of cancer
2-Designated as ‘ Natural’ as they don’t priming to kill infected cells unlike T cells

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11
Q

COMMON MEYLOID PROGENITOR- CMP

A

Precursor of erythrocytes, thrombocytes, granulocytes,
monocyte-macrophages, dendritic cells, mast cells and osteoclasts

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12
Q

MAST CELL

A

Long lived tissue resident cells
Functions include defense in parasitic infections and role in allergic reactions
Releases cytokines and inflammatory mediators

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13
Q

MYELOBLAST

A

UNIPOTENT STEM CELL
DIFFERENTIATES INTO VARIOUS EFFECTOR CELLS

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14
Q

BASOPHIL

A

Plays a role in:
Allergic reactions
Preventing blood clotting

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15
Q

EOSINOPHIL

A

Plays a role in defense against parasites

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16
Q

NEUTROPHIL

A

PHAGOCYTOSIS
BACTERICIDAL MECHANISMS

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17
Q

MONOCYTE

A

Phagocytic cells found in the blood stream
Matures into macrophages upon migration to tissues

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18
Q

MACROPHAGE- MAC

A

Phagocytosis
Bactericidal mechanisms
Antigen presentation

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19
Q

DENDENTIC CELLS

A

Antigen presentation
Initiation of activation of B and T cells

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20
Q

LYMPHOID ORGANS

A

PHOTO
Broadly subdivided into
Primary/Central Lymphoid Organs
Lymphocytes are generated
Ag cannot enter in
Secondary/Peripheral Lymphoid Organs
Adaptive immune responses are initiated
Lymphocytes are maintained
Ag can enter in

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21
Q

PRIMARY LYMPHOID ORGANS

A

Primary 2 Bone Marrow and Thymus
B and T cells originate in BM
Only B cells mature there; precursor T cells migrate to the thymus and undergo maturation there.
Mature B and T cells enter the bloodstream and
migrated to secondary/peripheral lymphoid organs:
Antigen cannot enter into these organs
They atrophy with age

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22
Q

SECONDARY LYMPHOID ORGANS

A

Specialized to:
- trap Ag-bearing dendritic cells
- Allow initiation of adaptive immune responses
- Provide signals that sustain recirculating
Lymphocytes
- Antigen can enter in
- Increase in size with age
- Includes
- Lymph nodes
- Spleen
- GALT, BALT & MALT

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23
Q

SECONDARY LYMPHOID ORGANS

A

Lymph nodes:
- Located at points of convergence of vessels of the lymphatic system
- Afferent lymphatics carry Ag-bearing cells from infected tissues to the LNs
- In LNs, B cells are localized in follicles while T cells are diffusely distributed
- This organization promotes interactions between APCs and T cells and between activated Ag-specific T cells and B cells
upon encountering Ag.

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24
Q

SECONDARY LYMPHOID ORGANS

A

+ Spleen
+ Collects Ag from the blood
+ Gut-associated lymphoid tissue
+ Includes tonsils, adenoids, appendix and patches in the small intestine

+ In 3H\HU·V patches, Ag collected by specialized epithelial cells: multi-
fenestrated or M cells

+ Bronchial-associated lymphoid tissue
+ Protects the respiratory epithelium
+ Mucosal-associated lymphoid tissue
+ Protects other mucosa

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25
Q

INNATE (EARLY) AND ADAPTIVE (LATER) BOTH HAVE ALPHA T CELL/ NK T CELL

A

INNATE IMMUNITY- RAPID RESPONSE CELLS INCLUDES: DENDENTIC CELL, MAST CELL,MACROPHAGES, NK CELLS, COMPLEMENT PROTEIN, EOSINOPHIL, NEURROPHIL, BASOPHIL, GRANDULOCYTES

26
Q

INNATE (EARLY) AND ADAPTIVE (LATER) BOTH HAVE ALPHA T CELL/ NK T CELL

A

INNATE IMMUNITY- RAPID RESPONSE CELLS INCLUDES: DENDENTIC CELL, MAST CELL,MACROPHAGES, NK CELLS, COMPLEMENT PROTEIN, EOSINOPHIL, NEURROPHIL, BASOPHIL, GRANDULOCYTES.

ADAPTIVE IMMUNITY (SLOW RESPONSE)
B CELL, T CELL- CD4+ CD8+, ANTIBODIES

27
Q

Innate (Early) Immune
System

A

The Innate Immune System
Detects pathogen-associated molecular patterns
(PAMPs) on surface of microbes via receptors called
Pattern Recognition Receptors (PRRs) Protects against
infection by removing the infectious agent
Microbes are able to evade innate defense systems
by changing their structure

28
Q

POINTS OF ENTRY
CELL TISSUES ORGANS

A

PHOTO
THYMUS, SPLEEN, LYMPH NODES, TONSILS AND ADENOIDS, LYMPH NODES, PEYER’S PATCH, BONE MARROW

29
Q

Pathogen Associated Molecular Patterns =
PAMPs

A

PHOTO
PARASITES- HELMINTHS- TAPEWORM
PROTOZOA- PLASMODIA-MALARIA
FUNGI- TINEA-ATHLETE’S FOOT
PROKARYOTE- BACTERIA- LEPROSY
VIRUS- HIV- AIDS
PRION-CJD

30
Q

Pathogen Associated Molecular Patterns =
PAMPs

A

BACTERIS GRAM +IVE AND -IVE> LIPOTEICHOIC ACID( LTA), PEPTIDOGLYCAN (PGN), LIPOPROTEINS, DNA, FLAGELLIN, LIPOPOLYSACCHARIDES (LPS)
VIRUS- COAT PROTEIN, NUCLEIC ACID
PARASITE- GPI ANCHOR
YEAST- ZYMOSAN (BETA-GLUCAN)

31
Q

Pattern Recognition Receptors
= PRRs

A

PHOTO
CLR
NLR
TLR
RLR

32
Q

WHAT IS INFLAMMATION

A

Clinically : The presence of
redness, swelling and pain
Histologically: The presence
of oedema fluid and the
infiltration of tissues by
leucocytes
Immunologically: Part of the
non-specific immune
response that occurs in
reaction to any type of
bodily injury

33
Q

ACUTE AND CHRONIC

A

Some infections cannot be cleared 2 Chronic inflammation e.g.
Tuberculosis, Hepatitis B
Acute & Chronic Inflammation
Mechanisms for responding to infections
Contributors to autoimmune disease

34
Q

WHAT ARE THE SIGNS OF INFLAMMATION

A

PHOTO

35
Q

5 CARDINAL SIGNS OF INFLAMMATION

A

PAIN HEAT REDNESS SWELLING LOSS OF FUNCTION

36
Q

ACUTE INFLAMMATION

A

Last a few days Lasts days to a few
weeks

Clearance highly dependent on
Innate Immune system +/- help from
adaptive immune system

E.g. Acute reactions to extracellular
bacteria result in pus formation 2 they
are Pyogenic
The yellow color is due to neutrophil granules.

Pus develops over a few hours
If the offending stimulus cannot be
removed, the inflammation becomes
chronic

37
Q

CHRONIC INFLAMMATION

A

Occurs when.
Infection difficult to clear. E.g. Chronic
intracellular bacterial infection may lead
to the formation of granuloma ( chronic
inflammatory lesion)
Persistence of foreign material, e.g. some
types of sutures
Immune system is attacking self tissue
(autoimmune disease)
Excessive formation & deposition of
endogenous material, e.g. urate crystals
in gout
T cells and macrophages are main cells
in chronic inflammatory lesions as
Granulomas
Adaptive immune response drives
chronic inflammatory responses

38
Q

WHAT ARE CYTOKINES

A

Soluble, low-molecular weight regulatory
proteins/glycoproteins secreted by cells, mainly
leucocytes, in response to stimuli, acting as intercellular
mediators or signaling molecules.

CYTOKINES CAN
Initiate acute
inflammation
Maintain chronic
inflammatory responses

Bind to specific receptors on target cells
Trigger signal-transduction pathways
Alter gene expression
Regulate the intensity and duration of the immune
response
Stimulate or inhibit the activation, proliferation and/or
differentiation of various cells
Regulate the secretion of Abs and other cytokines

Secreted transiently and their receptors are often
expressed transiently
Binding of a cytokine to its receptor stimulates increased
expression of the receptor and other cytokines

39
Q

INDUCTION AND FUNCTION OF CYTOKINES

A

PHOTO

40
Q

WHAT ARE THE ACTIONS OF CYTOKINES( WORK IN NETWORKS)

A

PHO

41
Q

A guide thru an immune
response

A

Inflammation can also be triggered by activation of
complement.
Complement coats microbial surfaces with fragments
that are recognised and bound by phagocytic receptors
on macrophages
Cytokines and complement fragments cause
circulating leucocytes to migrate to site of infection,
chemokines attract them there.

What is Complement?

42
Q

COMPLEMENT SYSTEM

A

A molecular barrier of the innate immune system
Nine basic complement components C1 to C9
Once activated, nine components split into smaller
fragments
Three pathways of Complement
Classical
Alternative
Lectin

43
Q

Physiologic - Extracellular Molecules -
Complement

A

PHO

43
Q

Physiologic 2 Extracellular Molecules 2
Complement Classical Pathway

A

PHOTO

Activated by IgG2 (IgG1,
IgG2, and IgG3 but not
IgG4) or IgM2containing
immune complexes
through binding by C1q.
C1qrs is then assembled
and cleaves complement
components C2 and C4
to form the C4b2a
enzyme complex, a C3
convertase.
Regulatory factors

MCP 2 membrane co-
factor protein

DAF 2 decay accelerating
factor
CD59 2 Prevents C9 from
completing MAC

44
Q

Physiologic 2 Extracellular Molecules 2
Complement Classical Pathway

A

PHOTO

Activated by IgG2 (IgG1,
IgG2, and IgG3 but not
IgG4) or IgM2containing
immune complexes
through binding by C1q.
C1qrs is then assembled
and cleaves complement
components C2 and C4
to form the C4b2a
enzyme complex, a C3
convertase.
Regulatory factors

MCP 2 membrane co-
factor protein

DAF 2 decay accelerating
factor
CD59 2 Prevents C9 from
completing MAC

45
Q

Physiologic 2 Extracellular
Molecules 2 Complement
Lectin Pathway

A

PHOTO

1) Activation of the lectin pathway is on the basis of recognition of microbial cell surface
carbohydrates by mannan-binding lectin
(MBL) or ficolin.
Lectin- carbohydrate binding protein
Ficolin- oligomeric lectins
MASP- MBL- associated
serine proteases
2) MBL binds to mannose
residues which activates
MASP1 & MASP2
3) This process leads to cleavage of C2 and C4 to form the classical pathway C3 convertase C4bC2a.)

46
Q

what is the complement cascade

A

photo

47
Q

ALTERNATIVE PATHWAY TO THE COMPLEMENT SYSTEM

A

PHOTOS

The alternative
pathway activates
complement on the
surface of any cell
that lacks
complement inhibitors,
whereas the lectin
and classical
pathways provide
focused complement
activation to
molecules that have
been bound by MBL or
antibody.

48
Q

ANTIGENS

A

Antigen- a substance
that induces an immune
response. Parts of an
antigen are recognized
by receptors of the
adaptive immune
system.
Can be classified
via how they induce
an immune
response and their
origins
Name the different
types of antigens

49
Q

ANTIGENS

A

PHOTO OF THE INNATE ADAPTIVE IMMUNITY PG 62
INNATE IMMUNITY- MICROBE - EPITHELIAL BARRIER, NEUYROPHIL, MACROPHAGES, NK CELL, COMPLEMENT, NATURAL ANTIBODIES
ADAPTIVE IMMUNITY- B LYMPHOCYTE, HELP T LYMPHOCYTE,CYTOTOXIC T YMOHOCYTE, HIGH AFFINITY ANTIBODIES

50
Q

THE ADAPTIVE IMMUNITY SYSTEM

A

T and B lymphocytes 2 main immune cells
Large numbers of pre-existing receptors expressed on
lymphocytes 2 potential to bind with any foreign Ag entering the body
Three groups of molecules specifically recognize foreign
Ag:
T cell receptor (TCR)
B cell receptor (BCR)
Major Histocompatibility complex (MHC) 2 the cluster of
genes is known as human leukocyte Ag (HLA) in humans

51
Q

THE ADAPTIVE IMMUNE SYSTEM

A

7DQG%FHOOVμVHHμ
antigen differently

B cells can bind directly
with bits of the antigen

T cells see bits of antigen
bound to MHC molecules

Antigen presenting cells
“ chew: antigen and put these fragment into MHC molecules on their surfaces.
fragment into MHC molecules
on their surfaces

52
Q

Physiologic 2 Extracellular Molecules 2
Complement Alternative Pathway

A

photo

1) Initiated constantly by
spontaneous hydrolysis of C3,
leading to the formation of
C3(H2O)Bb, which cleaves C3
into C3a and C3b.
3) Amplification of this pathway is
on the basis of the covalent
binding of C3b to activating
surfaces (e.g., bacterial
surface) followed by cleavage
of factor B (FB).
3) In the presence of factor D and
properdin, this process leads to
formation of the alternative
pathway C3 convertase
(C3bBb).
4) Properdin promotes association
between C3b and FB, thus
stabilizing the alternative
pathway C3 convertase
(C3bBb).
Regulatory factors
- Factor H
- Factor I
- CR1

53
Q

Antibodies ( serum Ig )

A

photo

54
Q

MHC l AND ll CLASSES

A

photo

55
Q

immunoglobulin (IgG)

A

photo

56
Q

antibodies

A

photo of the five different classes of an antibodies

The five different classes of human heavy chains have
slightly different structures.
Each class is designated by lowercase Greek letters:
- IgMǍ- IgM
- IgD
- IgG
- IgE
- IgA

57
Q

TCRs 2 classes of T- cell receptor

A

photo pg 69
antigen-binding site alpha and beta chain

58
Q

IMMUNOLOGIC MEMORY

A

Long-term immunologic memory
2 capacity to generate an
enhanced and more effective
immune response to an Ag
encountered in the past .

Naïve B cells activated by Ag
differentiate in Plasma Cells that
secrete Ab

In a primary response the plasma cells
secrete a relatively low affinity Ab
In a secondary response a higher affinity
Ab is secreted -

59
Q

IMMUNOLOGIC MEMEORY

A

PHOTO 71
Primary response Secondary
Response

Time period to
response

5 2 10 days 1 2 3 days

Antibody class Mainly IgM IgG, IgA or IgE

Affinity for Ag Low High