Last edited: 8/9/2021

INFLAMMATION: VASCULAR EVENTS

Immunology: Inflammation: Vascular Events Medical Editor: Dr. Sofia Suhada M. Uzir

OUTLINE (A) THE CASCADE OF EVENTS

• The chemicals from tissue injuries trigger a cascade of
I) SURFACE BARRIERS events including:
II) INTRODUCTION TO INFLAMMATION
(1) Vasodilation of blood vessels
III) VASCULAR EVENTS IN INFLAMMATION
● ↑ blood flow to area where pathogen is
IV) REVIEW QUESTIONS o This ↑ in blood flow causes redness and heat to area
V) REFERENCES of injury

I) SURFACE BARRIERS (2) ↑ Vascular permeability

● Causes plasma proteins and WBCs to leak out of blood
SURFACE vessel and into tissue space where pathogen is
MECHANISM OF ACTION o This ↑ permeability → swelling and pain
BARRIER
ACID MANTLE Sweat and sebum ● Pain also occurs due to nerve ending activation by
OF SKIN • ↑ Acidity of the skin chemicals listed above
• ↓ Bacterial growth
• Contain bactericidal chemicals
(defensins)

KERATIN IN Keratin
SKIN • Resistant to acids
• Resistant to alkali (base)
• Resistant to bacterial enzymes

MUCUS Traps pathogens in respiratory and

GIT
NASAL HAIRS Filters and traps pathogens in nasal
cavity
CILIA Propel pathogens and cellular debris
away from nasal cavity and Lower
respiratory tract
GASTRIC Contains HCL and pepsin that
JUICE destroy pathogens in stomach
ACID MANTLE Acidity → inhibits growth of fungi and
OF VAGINA bacteria Figure 1 Vascular cascade; increase in blood flow due to
tissue inflammation [ResearchGate]
LACRIMAL • Contains Lysozymes → destroys
FLUID & pathogenic microorganisms
SALIVA (3) ↑ Expression of adhesion molecules
• Contains Lactoferrin → ↓ iron
utilization for bacteria ● For WBCs to exit blood vessels and into tissue spaces
where pathogen is
URINE Acidic pH → ↓ bacterial growth and
keeps Lower Urinary Tract clean (i) Expressed in the early stages of inflammation:
 P-selectins
• Bind WBCs Sialyl-Lewis molecules and keep
II) INTRODUCTION TO INFLAMMATION them close to blood vessel wall (margination)
 PE-cams
● Define
• Allow WBCs to move between endothelial
o Any type of tissue damage that initiate vascular or
cells of blood vessel (diapedesis)
cellular events which cleans up any cellular
pathogens → initiate repair (ii) Expressed in the late stages of inflammation:
● Causes of inflammation include: ● After WBCs come to area of Injury, they release IL-1/IL-
o Physical trauma 8/TNF-alpha → leads to adhesion molecule expression
o Chemical trauma
 E-selectins
o Infectious microorganisms
• Bind WBCs Sialyl-Lewis molecules and keep
o Sunlight/burns
them close to blood vessel wall (margination)
III) VASCULAR EVENTS IN INFLAMMATION  I-Cams/ V-Cams
• Bind integrins of WBCs circulating in blood
• Tissue injury from pathogens → Triggers injured vessel and hold them tight against blood
tissues, endothelial cells, platelets, basophils and mast vessel wall (Tight Binding)
cells to release:
 PE-Cams
o Histamines
o Serotonin • Allow WBCs to move between endothelial
o Prostaglandins cells of blood vessel (diapedesis)
o Bradykinins
o Leukotrienes

INFLAMMATION: VASCULAR EVENTS IMMUNOLOGY: Note #1. 1 of 2

(4) Movement of WBCs toward pathogen IV) REVIEW QUESTIONS
● After they enter tissue space (positive chemotaxis/
The first vascular response to injury is
migration)
a. Slowing the circulation
o Leukotrienes, C5a, IL-8 and platelet activating factor
b. Venular dilatation
→ trigger WBCs to move towards pathogen (like c. Recruitment of the vascular beds
leaving a cookie trail towards pathogen) d. Capillary enlargement
e. Arteriolar vasoconstriction
(5) Activated WBCs

● Start releasing more IL-1/TNF-alpha → stimulates liver, Which of the following triggers release of acute
phase reactant proteins?
brain, ted bone marrow a. Leukotrienes
(i) Liver: b. Ferritin
c. Liver
 Triggers release of acute phase reactant proteins
d. Blood vessels
• IL-6
• Ferritin
Which of the following immune cells is unable to
• Fibrinogen phagocytose?
• Haptoglobin a. Neutrophils
• CRP b. Basophils
• Ceruloplasmin c. Eosinophils
(ii) Brain d. Monocytes
e. Macrophages
 Triggers hypothalamus → sympathetic division
activated →↑body temperature → fever Macrophages are derived from
a. Monocytes
(iii) Red Bone marrow b. T cells
c. B cells
 Along with IL-1/TNF-alpha there is also IL-3/ IL-5
d. Eosinophils
and many other that →↑ WBC formation e. Plasma cells
(leukocytosis)
Regarding the chemical mediators of inflammation
a. Histamine is derived from plasma
b. C3b is within macrophages
c. The kinin system is activated in platelets
d. Nitric oxide is preformed in leukocytes
e. Serotonin is preformed in mast cells

Which of the following is included in the cascade of

events during an inflammation?
a. Vasoconstriction of blood vessels
b. Decrease in body temperature
c. Increase in vascular permeability
d. Increase in heat to the area of injury

Which of the following are increased when tissue

injury occurs?
a. Insulin
b. Serotonin
c. Pepsin
d. Bilirubin

CHECK YOUR ANSWERS

Figure 2 Summary of vascular events in inflammation
[University of Western Australia]
V) REFERENCES
● Le T, Bhushan V, Sochat M, Chavda Y, Zureick A. First Aid for
the USMLE Step 1 2018. New York, NY: McGraw-Hill Medical; 2017
● Marieb EN, Hoehn K. Anatomy & Physiology. Hoboken, NJ:
Pearson; 2020.
● Boron WF, Boulpaep EL. Medical Physiology.; 2017.
● Urry LA, Cain ML, Wasserman SA, Minorsky PV, Orr RB,
Campbell NA. Campbell Biology. New York, NY: Pearson; 2020.
● Jameson JL, Fauci AS, Kasper DL, Hauser SL, Longo DL,
Loscalzo J. Harrison's Principles of Internal Medicine. New York
etc.: McGraw-Hill Education; 2018.
● Iberts B, Johnson A, Lewis J, Raff M, Roberts K, Walter P . Molecular
Biology of the Cell. New York, NY: Garland Science; 2002
● Murphy K, Weaver C. Janeway's Immunobiology. Garland
Science; 2016
● Doan T, Melvold R, Viselli S, Waltenbaugh C. Immunology.
Lippincott Williams & Wilkins; 2012
● Levinson W. Review of Medical Microbiology and Immunology.
Lange; 2012
● Soman N Abraham. ResearchGate [digital image] Retrieved
from: https://www.researchgate.net/figure/Local-effect-of-MCs-on-
the-vasculature-during-acute-inflammation-In-this-
diagram_fig3_51639881; 2011
● The University of Western Australia. [digital image] from:
www.meddent.uwa.edu.au/__data/assets/pdf_file/0018/3036123/PA
TH2220-2017-Lecture-4-Inflammation-1.pdf

2 of 2 IMMUNOLOGY: Note #1. INFLAMMATION: VASCULAR EVENTS

 Last edited: 8/9/2021

INFLAMMATION: CELLULAR EVENTS

Immunology: Inflammation: Cellular Events Medical Editor: Dr. Sofia Suhada M. Uzir

OUTLINE
I) OVERVIEW – EVENTS IN INFLAMMATION
II) REVIEW QUESTIONS
III) REFERENCES

I) OVERVIEW – EVENTS IN INFLAMMATION

● WBCs leave blood and enter tissue spaces → where

pathogen is, and this leads to different cellular events
including phagocytosis and nonspecific pathogen killing

(A) PHAGOCYTOSIS
● This process is mainly carried out by neutrophils and
macrophages
● Neutrophils and macrophages perform phagocytosis of
pathogen taking pathogen into cell
→ forming a phagosome → this combines with
lysosomes (have specific types of hydrolytic
enzymes) in cells → forming a phagolysosome Figure 1. Phagocytosis after an injury [Lumen Learning]

→ lysosomal enzymes break down pathogen (2) Macrophages

macromolecules into small pieces (antigens) ● In macrophages these antigens may be expressed on
MHC II molecules on cell surface
(1) Neutrophils o These macrophages are referred to as Antigen
● In neutrophils these antigens are exocytosed into Presenting cells (APCs) → these APCs then interact
interstitial fluid and then carried to nearby lymph nodes with T-helper cells
● Neutrophils also kill these pathogens in the ● These will later on also go to the nearby lymph nodes
phagolysosome via respiratory burst
(i) Antigen Presenting cells (APCs)
(i) Mechanism
o Macrophages
o The neutrophils use reactive oxygen species like o Dendritic Cells
H202 to make HOCL via an enzyme called o B-cells
myeloperoxidase
o This HOCL destroys the pathogens but in the process
HOCL molecules also destroy neutrophils as well →
leading to DNA of neutrophil being released out of
cell
→ This DNA binds to other pathogens in a net like
fashion (neutrophil extracellular trap) → this
enhances other WBCs to phagocytose that
tagged pathogen

Figure 2. Inflammatory response showing macrophages and

neutrophils acting on pathogens [Biology exams 4 U]

INFLAMMATION: CELLULAR EVENTS IMMUNOLOGY: Note #1. 1 of 3

 (B) NONSPECIFIC PATHOGEN KILLING
(1) Natural killer cells
● Activation of natural killer cells
(i) Through MHC I complex
● If a viral pathogen infects tissue cells
→ virus induces abnormal MHC I complex or inhibit MHC
I formation
o This foreign MHC I or absent MHC I due to viral
infection → activates natural killer cells
o The activated natural killer cells → release perforins
and granzymes which trigger apoptosis of viral
infected cells
(ii) Via antibody dependent cell mediated
cytotoxicity
● If IgG antibodies made by plasma cells bind viral antigens
expressed on MHC I complex
→ This allows natural killer cells to bind to Fc portion of
IgG antibody via their CD-16 protein
→ This activates the natural killer cells
o The activated natural killer cells then release perforins
and granzymes which trigger apoptosis of viral
infected cells

Figure 3. Direct and indirect activation of NK cells

[Frontiers in Immunology]

2 of 3 IMMUNOLOGY: Note #1. INFLAMMATION: CELLULAR EVENTS

 II) REVIEW QUESTIONS III) REFERENCES
● Amir Horowitz, Kerstub A. Stegnabb abd Ekeabir M. Riley.
Which refers to swelling as a result of inflammation?
Activation of natural killer cells during microbial infections. [Digital
a. Erythema image] https://internal-
b. Edema journal.frontiersin.org/articles/10.3389/fimmu.2011.00088/full 2012.
c. Granuloma ● Biology Exams 4 U [Digital image]
https://www.biologyexams4u.com/2012/11/immunology-
d. Vasodilation inflammatory-response.html
● Lumen Microbiology Course [Digital image]
Which type of inflammation occurs at the site of an https://courses.lumenlearning.com/microbiology/chapter/inflammatio
injury or infection? n-and-fever/
a. Acute ● Cara Splash. Inflammation Quiz. 2021
b. Chronic https://www.funtrivia.com/playquiz/quiz28640520ca160.html
● Le T, Bhushan V, Sochat M, Chavda Y, Zureick A. First Aid for
c. Endogenous the USMLE Step 1 2018. New York, NY: McGraw-Hill Medical; 2017
d. Exogenous ● Marieb EN, Hoehn K. Anatomy & Physiology. Hoboken, NJ:
Pearson; 2020.
Which of these processes is NOT one of the cellular ● Boron WF, Boulpaep EL. Medical Physiology.; 2017.
events involved in the inflammatory process? ● Urry LA, Cain ML, Wasserman SA, Minorsky PV, Orr RB,
Campbell NA. Campbell Biology. New York, NY: Pearson; 2020.
a. Margination
● Jameson JL, Fauci AS, Kasper DL, Hauser SL, Longo DL,
b. Diapedesis Loscalzo J. Harrison's Principles of Internal Medicine. New York
c. Selection etc.: McGraw-Hill Education; 2018.
d. Rolling ● lberts B, Johnson A, Lewis J, Raff M, Roberts K, Walter P .
Molecular Biology of the Cell. New York, NY: Garland Science;
Which of the following is NOT and antigen 2002
● Murphy K, Weaver C. Janeway's Immunobiology. Garland
presenting cells? Science; 2016
a. Macrophages ● Doan T, Melvold R, Viselli S, Waltenbaugh C. Immunology.
b. Dendritic Cells Lippincott Williams & Wilkins; 2012
● Levinson W. Review of Medical Microbiology and Immunology.
c. B-Cells
Lange; 2012
d. T-cells
Which of the following processes is not a step in
phagocytosis?
a. Recognition
b. Adhesion
c. Engulfment
d. Degradation
What is the name of the enzyme involve in
neutrophil’s reaction during an inflammation?
a. Myroxomes
b. Myeloperoxidase
c. Perforins
d. Granzymes
Which statement is incorrect regarding
macrophages?
a. It has no role during an inflammatory response
b. It may be expressed on MHC II molecules
c. It is considered as an APCs
d. It interacts with T-helper cells during an inflammation
Regarding nonspecific pathogen killing, which is
true?
a. The virus induces abnormal MHC II complex or
inhibit MHC II formation
b. It has no role in antibody dependent cell mediated
cytotoxicity
c. Perforins and granzymes are released
d. It inactivates natural killer cells
Regarding perforins, which is true?
a. It is activated by neutrophils
b. It triggers apoptosis of viral infected cells
c. It triggers hemolysis of blood cells
d. It is phagocytosed by the macrophages
Which of the following statements regarding IgG
antibodies are correct?
a. It helps release myeloperoxidase enzymes
b. It helps phagocytosis of viral infected cells through
the release of neutrophils
c. It is made by plasma cells
d. It helps in regulation of body temperature when
inflammation occurs

CHECK YOUR ANSWERS

INFLAMMATION: CELLULAR EVENTS IMMUNOLOGY: Note #1. 3 of 3

 Last edited: 8/9/2021

INFLAMMATION: COMPLEMENT PROTEINS

Immunology: Inflammation: Complement Proteins Medical Editor: Dr. Sofia Suhada M. Uzir

OUTLINE (B) ALTERNATIVE PATHWAY

I) OVERVIEW (1) Through C3b molecule

II) CASCADE PATHWAYS ● C3b molecules bind directly to lipopolysaccharides on
III) REVIEW QUESTIONS bacteria → this causes alternative complement cascade

IV) REFERENCES Remember:

● C3b → this triggers opsonization (makes the pathogen
tasty, YUM)
I) OVERVIEW o → enhances phagocytosis of microbe
● Proteins made by liver in inactive form ● If Bb protein binds with C3b
● It is a part of the innate immune system (nonspecific) o →this activates binding of C5b→C6→C7→C8→C9
● Normally circulating in the plasma ● C5b-C9 → triggers formation of membrane attack complex
o Inflammation response causes ↑ vascular (MAC)
permeability → complement proteins leave blood and o → this binds into bacteria →causing lysis of bacterial
enter tissue where pathogens are cell
→ triggers complement cascade pathways ● C3 and C5 → break up into C3a & C5a as well as C3b &
C5b
II) CASCADE PATHWAYS o C3a & C5a →↑ Chemotaxis and amplifies inflammatory
response
(A) CLASSICAL PATHWAY
(1) Definition
● Antigen-antibody mediated
● C1 molecules bind Fc portion of IgG
● IgM antibodies made by plasma cells bind microbe
antigens
→ this causes classic complement cascade
(2) Through C1 activation
● C1 activates
o C2b→C4b→C3b→C5b→C6→C7→C8→C9

Remember:
● If the pathway stops at C3b → this triggers opsonization
(makes the pathogen tasty, YUM)
→ enhances phagocytosis of microbe
● If the pathway goes to C5b-C9 → this triggers formation of
membrane attack complex (MAC)
Figure 2. Alternative pathway of complement cascade
→ this binds into bacteria creating pores → causing lysis [Wikipedia]
of bacterial cell
● C3b → opsonization
o Enhance phagocytosis via C3b receptor
● C3 and C5 → break up into C3a & C5a as well as C3b &
C5b
o C3a & C5a → can be acted by the proteases secreted
by mass cells → conversion C3a and C5a into the active
form → ↑ Chemotaxis and amplifies inflammatory
response

Figure 1. Classical complement pathway [Wikipedia]

INFLAMMATION: COMPLEMENT PROTEINS IMMUNOLOGY: Note #1. 1 of 3

 (C) LECTIN PATHWAY
(1) Through C4 molecule
● C4 molecules bind directly to mannose or other sugar
residues on bacteria
● C1 like complex converts C4 into C4b
o This triggers lectin complement cascade

Remember:
● C4b activates → C3b→C5b→C6→C7→C8→C9
● C3b → triggers opsonization (makes the pathogen tasty,
YUM)
o → enhances phagocytosis of microbe
● C5b-C9 → triggers formation of membrane attack complex
(MAC)
o → this binds into bacteria → causing lysis of bacterial
cell
● C3 and C5 → break up into C3a & C5a as well as C3b &
C5b
o C3a & C5a→ ↑ Chemotaxis and amplifies inflammatory
response

Figure 3. Complement cascade [Wikipedia]

Figure 4. Summary of the complement cascade [MicrobeOnline]

2 of 3 IMMUNOLOGY: Note #1. INFLAMMATION: COMPLEMENT PROTEINS

 III) REVIEW QUESTIONS
Which of the following complement component
Complements are the proteins that are involved in facilitate opsonization and phagocytosis?
the clearance of antigens/bacteria. Which of the a. C3a
following pathway is involved in the adaptive b. C3b
immune response? c. C5a
a. Alternative Pathway d. C5b
b. Classical Pathway
c. Lectin Binding Pathway
The deficiency of the complement proteins (C1q,
d. All of the above
C1q, C1s) or the complement receptors lead to the
accumulation of immune complexes resulting in
In the classical pathway, the antibody activated the SLE or vasculitis. The deficiency affects the
C1 complex consisting of C1q, C1r & C1s subunit. following complement pathway
Which of the following subunit binds to the a. Alternative pathway
antibody? b. Classical pathway
a. C1q c. Lectin binding pathway
b. C1r d. None of the above
c. C1s
d. All of the above
CHECK YOUR ANSWERS
Which of the following isotype antibody is a potent
activator of the classical complement pathway?
IV) REFERENCES
a. IgM
b. IgA ● Hduman Galician. Complement Pathway [Digital image]
https://en.m.wikipedia.org/wiki/Complement_system#/media/File%3
c. IgE AComplement_pathway.svg
d. IgG ● Srijana Khanal. Complemetn pathway; Types, Functions,
Regulations. [Digital image] https://microbeonline.com/complement-
system-pathways-functions-regulation/
In the classical pathway, which of the following ● Medicalbiochemist [Quiz]
https://www.medicalbiochemist.com/2019/04/mcq-complement-
complement complex serve as C3 convertase?
pathway.html
a. C4aC2a ● Le T, Bhushan V, Sochat M, Chavda Y, Zureick A. First Aid for
b. C4bC2b the USMLE Step 1 2018. New York, NY: McGraw-Hill Medical; 2017
c. C4bC2a ● Marieb EN, Hoehn K. Anatomy & Physiology. Hoboken, NJ:
Pearson; 2020.
d. C4aC2b ● Boron WF, Boulpaep EL. Medical Physiology.; 2017.
● Urry LA, Cain ML, Wasserman SA, Minorsky PV, Orr RB,
Campbell NA. Campbell Biology. New York, NY: Pearson; 2020.
Which of the following process is required for the ● Jameson JL, Fauci AS, Kasper DL, Hauser SL, Longo DL,
formation of C3 convertase that amplifies Loscalzo J. Harrison's Principles of Internal Medicine. New York
etc.: McGraw-Hill Education; 2018.
complement activation?
● lberts B, Johnson A, Lewis J, Raff M, Roberts K, Walter P .
a. C3b must bind to foreign antigens Molecular Biology of the Cell. New York, NY: Garland Science;
b. Factor B must bind to C3b for its proteolysis by 2002
Factor D ● Murphy K, Weaver C. Janeway's Immunobiology. Garland
Science; 2016
c. Properdin must bind to the C3bBb complex for ● Doan T, Melvold R, Viselli S, Waltenbaugh C. Immunology.
stabilization Lippincott Williams & Wilkins; 2012
d. All of the above ● Levinson W. Review of Medical Microbiology and Immunology.
Lange; 2012

Certain microorganism such as Salmonella, Listeria,

Neisseria, Cryptococcus consist of specific
carbohydrate moieties on the surface antigen that
activate
a. Alternative Pathway
b. Classical Pathway
c. Lectin Binding Pathway
d. All of the above

Which of the following complement protein

polymerizes to form perforin like structure that
stabilizes membrane attack complex.
a. C6
b. C7
c. C8
d. C9
Which of the following component of complement
proteins enhances inflammation (anaphylatoxin)?
a. C3a
b. C5a
c. Both of the above
d. None of the above

INFLAMMATION: COMPLEMENT PROTEINS IMMUNOLOGY: Note #1. 3 of 3

 Last edited: 8/8/2021

TOLL-LIKE RECEPTORS AND INTERFERONS

Immunology: Inflammation: Toll-like Receptors and Interferons Medical Editor: Dr. Sofia Suhada M. Uzir

OUTLINE II) INTERFERONS

I) TOLL-LIKE RECEPTORS ● Proteins made by virus infected cells
II) INTERFERONS ● Functions:
o Signal nearby host cells, let them know that there’s a
III) REVIEW QUESTIONS virus in the vicinity→ make antiviral peptides
IV) REFERENCES o Alerting macrophages and natural killer cell to
become activated and proliferate
● Virus infects cells
I) TOLL-LIKE RECEPTORS o Triggers virus infected cell to express genes for
interferon production
● Proteins present in the cell membrane/vesicles inside the
cells that respond to foreign pathogens → elicit specific ● Interferon (IFN) types
responses o Alpha & beta IFNs
● Receptors expressed on WBCs like macrophages o Gamma IFNs
● These receptors bind various pathogen associated
(A) ALPHA & BETA INTERFERONS
molecular proteins (PAMPs)
● Tell nearby healthy cells that there is a virus in the vicinity
(1) PAMPs ● The nearby healthy cells than ↑ expression of antiviral
o Detail viral nucleic acids (RNA and DNA) peptides
o Lipopolysaccharide on bacteria o If virus does infect healthy cells these antiviral
o Flagellin on bacteria nucleases will destroy viral nucleic acids
● When these receptors are activated by these PAMPs ● These IFNs also cause cells to ↑ expression of viral
o → triggers WBC to increase expression of nuclear antigens on MHC I molecules to activate cytotoxic T-cells
factor kappa beta (NfKB) →↑ expression of
proinflammatory cytokines such as: (B) GAMMA INTERFERONS
 IL-1 Beta ● These are made by natural killer cells and T helper type 1
 IL-18 cells when stimulated by IL-12 from activated
 TNF-alpha macrophages
 Interferons ● Actions:
o ↑ activity of macrophages → ↑ phagocytosis of virus
o ↑ activity of natural killer cells →↑cell killing of virus
infected cells
o ↑ expression of viral antigens on MHC II molecules for
antigen presentation to trigger ↑ antibody production
against virus

Figure 1. PAMPs recognition by TLRs [Hindawi]

Figure 2. Interferon functions [LSE]

TOLL-LIKE RECEPTORS AND INTERFERONS IMMUNOLOGY: Note #1. 1 of 2

 III) REVIEW QUESTIONS IV) REFERENCES
● Asa Cusack. The London School of Economics and Political
Which of the following IS NOT a proinflammatory
Science. Interferon functions [Digital image] LSE
cytokines? ● Ji-Yoon Noh, Suk Ran Yoon, Tae-Don Kim, Inpyo Choi,
a. IL-1 beta Haiyoung Jung, "Toll-Like Receptors in Natural Killer Cells and
b. TNF-alpha Their Application for Immunotherapy", Journal of Immunology
Research, vol. 2020, Article ID 2045860, 9 pages, 2020.
c. TNF-delta [Digital image] https://www.hindawi.com/journals/jir/2020/2045860/
d. IL-18 ● Le T, Bhushan V, Sochat M, Chavda Y, Zureick A. First Aid for
the USMLE Step 1 2018. New York, NY: McGraw-Hill Medical; 2017
● Marieb EN, Hoehn K. Anatomy & Physiology. Hoboken, NJ:
Concerning PAMPs, which is true? Pearson; 2020.
a. The toll like receptors decrease its amount ● Boron WF, Boulpaep EL. Medical Physiology.; 2017.
b. Lipopolysaccharide on RNA is an example ● Urry LA, Cain ML, Wasserman SA, Minorsky PV, Orr RB,
Campbell NA. Campbell Biology. New York, NY: Pearson; 2020.
c. Flagellin on virus is an example ● Jameson JL, Fauci AS, Kasper DL, Hauser SL, Longo DL,
d. Flagellin on bacteria is an example Loscalzo J. Harrison's Principles of Internal Medicine. New York
etc.: McGraw-Hill Education; 2018.
● lberts B, Johnson A, Lewis J, Raff M, Roberts K, Walter P .
Which of the following is not a type of interferons?
Molecular Biology of the Cell. New York, NY: Garland Science;
a. Alpha 2002
b. Beta ● Murphy K, Weaver C. Janeway's Immunobiology. Garland
c. Gamma Science; 2016
● Doan T, Melvold R, Viselli S, Waltenbaugh C. Immunology.
d. Delta Lippincott Williams & Wilkins; 2012
● Levinson W. Review of Medical Microbiology and Immunology.
Which of the following is true concerning the Lange; 2012
actions of interferons?
a. Increase activity of macrophages
b. Decrease expression of viral antigens on MHC II
molecules
c. Alerting nearby healthy cells to initiate apoptosis
d. Alerting nearby healthy cells to release macrophages

Regarding alpha interferons, which is true?

a. It is considered as the late acting interferons
b. It helps in stimulating macrophages
c. It works by attaching to gamma interferons
d. It helps in activating cytotoxic T-cells

Regarding gamma interferons, which is true?

a. It directly activates cytotoxic T-cells
b. It helps increase cell expression of viral antigens on
MHC I molecules
c. It is made by natural killer cells
d. It doesn’t increase the activity of macrophages

Interferons are special defense mechanism which

operates by
a. Binding to viruses
b. Binding to neighboring cells
c. Producing a long-lasting state of resistance
d. Inhibiting virus induced enzymes

Cytotoxic T-cells can be activated via which of the

following?
a. By reacting with budding viruses
b. By identifying virus peptides presented by antibodies
c. By identifying virus peptides presented by MHC I
d. By releasing complement

How are antibody producing cells stimulated?

a. Interacting with a virus short peptide
b. Interacting with a T helper cell
c. Interacting with a plasma cell
d. Interacting with a virus infected cell

Which of the following is a characteristic of toll-like

receptors?
a. Cytoplasmic pattern recognition receptors
b. Type 1 membrane proteins consisting of a
recognition and signaling domain
c. Highly conserved receptors involved in programmed
cell death
d. Promotes activation of the transcription factor NFAT
(nuclear factor of activated T cells)

CHECK YOUR ANSWERS

2 of 2 IMMUNOLOGY: Note #1. TOLL-LIKE RECEPTORS AND INTERFERONS