Last edited: 8/8/2021

IMMUNE SYSTEM OVERVIEW

Immunology: Immune System: Overview Medical Editor: Dr. Sofia Suhada M. Uzir

OUTLINE (3) ↑ Expression of adhesion molecules

I) INNATE IMMUNE SYSTEM ● For WBCs to exit blood vessels and into tissue spaces
where pathogen is
II) ADAPTIVE IMMUNITY
III) NATURAL KILLER CELLS (i) Expressed in the early stages of inflammation:
 P-selectins
IV) MAJOR HISTOCOMPATIBILITY COMPLEXES
• Bind WBCs Sialyl-Lewis molecules and keep
V) CYTOKINES them close to blood vessel wall (margination)
VI) INTERLEUKINS  PE-cams
• Allow WBCs to move between endothelial
VII) TUMOR NECROSIS FACTOR ALPHA cells of blood vessel (diapedesis)
VIII) TRANSFORMING GROWTH FACTORS (TGF)
(ii) Expressed in the late stages of inflammation:
IX) QUESTIONS
 E-selectins
X) REFERENCES • Bind WBCs Sialyl-Lewis molecules and keep
them close to blood vessel wall (margination)
 I-Cams/ V-Cams
I) INNATE IMMUNE SYSTEM • Bind integrins of WBCs circulating in blood
vessel and hold them tight against blood
• Damage from the bacteria cell → Triggers the release
vessel wall (Tight Binding)
of endotoxins → release of cytokines:
o Histamines  PE-Cams
o Serotonin • Allow WBCs to move between endothelial
o Prostaglandins cells of blood vessel (diapedesis)
o Bradykinins (4) Movement of WBCs toward pathogen
o Leukotrienes
● After they enter tissue space (positive chemotaxis/
(A) VASCULAR EVENTS migration)
• The chemicals from tissue injuries trigger a cascade of o Leukotrienes, C5a, IL-8 and platelet activating factor
events including: → trigger WBCs to move towards pathogen (like
(1) Vasodilation of blood vessels leaving a cookie trail towards pathogen)

● ↑ blood flow to area where pathogen is (5) Activated WBCs

o This ↑ in blood flow causes redness and heat to area
● Start releasing more IL-1/TNF-alpha → stimulates liver,
of injury
brain, ted bone marrow
(2) ↑ Vascular permeability
(i) Liver:
● Causes plasma proteins and WBCs to leak out of blood
 Triggers release of acute phase reactant proteins
vessel and into tissue space where pathogen is
o This ↑ permeability → swelling and pain • IL-6
• Ferritin
● Pain also occurs due to nerve ending activation by • Fibrinogen
chemicals listed above • Haptoglobin
• CRP
• Ceruloplasmin
(ii) Brain
 Triggers hypothalamus → sympathetic division
activated →↑body temperature → fever

(iii) Red Bone marrow

 Along with IL-1/TNF-alpha there is also IL-3/ IL-5
and many other that →↑ WBC formation
(leukocytosis)

CELLULAR EVENTS

● WBCs leave blood and enter tissue spaces → where

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

Figure 1 Vascular cascade; increase in blood flow due to
tissue inflammation [ResearchGate]
(B) PHAGOCYTOSIS
● This process is mainly carried out by neutrophils and
macrophages
● Neutrophils and macrophages perform phagocytosis of
pathogen taking pathogen into cell

IMMUNE SYSTEM OVERVIEW IMMUNOLOGY: Note #1. 1 of 7

 → forming a phagosome → this combines with  Antibody mediated
 C1 → C9
lysosomes in cells → forming a phagolysosome
 Produces C3 and C5
→ lysosomal enzymes break down pathogen
• Enhance inflammation
macromolecules into small pieces (antigens) o Alternative
 Not antibody mediated
(1) Neutrophils
• C3 bind directly with the formed pathogen
● In neutrophils these antigens are exocytosed into
● The overall cascade causes production of:
interstitial fluid and then carried to nearby lymph nodes
o Membrane attack complexes
● Neutrophils also kill these pathogens in the
o Initiate lysis of bacteria, enhance opsonization by the
phagolysosome via respiratory burst
C3b
(i) Mechanism o Enhance inflammatory response through C3a and
o The neutrophils use reactive oxygen species like C5b
H202 to make HOCL via an enzyme called
INTERFERONS
myeloperoxidase
o This HOCL destroys the pathogens but in the process ● Proteins made by virus infected cells
HOCL molecules also destroy neutrophils as well → ● Virus Infects cells
leading to DNA of neutrophil being released out of o Triggers Virus Infected cell to express Genes for
cell Interferon Production

→ This DNA binds to other pathogens in a net like ● Interferon (IFN) types:
fashion (neutrophil extracellular trap) → this (3) Alpha & beta IFNs
enhances other WBCs to phagocytose that tagged
● Produced by different types of cells
pathogen
o Beta interferons is specifically made by platelets
● Tell nearby healthy cells that there is a virus in the vicinity
● The nearby healthy cells then increase expression of
antiviral peptides (example: protein kinase R)
● If virus does infect healthy cells these antiviral nucleases
will destroy viral nucleic acids/ prevent the virus from
attaching
o This prevents from damaging the tissue cells
● They can also cause activation of natural killer cells
(4) Gamma IFNs
● These are made by natural killer cells and T helper
type 1 cells when stimulated by IL-12 from activated
macrophages
● These IFNs Increase activity of macrophages
o ↑ phagocytosis of virus
● These IFNs Increase activity of natural killer cells
o ↑cell killing of virus infected cells
● These IFNs increase expression of viral antigens on MHC
II molecules for antigen presentation to trigger increased
antibody production against virus
Figure 2. Phagocytosis after an injury [Lumen Learning] TOLL LIKE RECEPTORS
● The overall results of toll like receptors is productions of
(2) Macrophages
o Specific types of signaling proteins for chemotaxis
● In macrophages these antigens may be expressed on o Interferons
MHC II molecules on cell surface o Preform of tumor necrotic alpha, IL-1 beta, IL-18
o These macrophages are referred to as Antigen  Have to be activated by caspases
Presenting cells (APCs) → these APCs then interact
● Enhance inflammatory response and chemotaxis →
with T-helper cells
eliminate more pathogens from the body
(i) Antigen Presenting cells (APCs)
II) ADAPTIVE IMMUNITY
o Macrophages
o Dendritic Cells ● By exocytosis → Antigens released from neutrophils
o B-cells ● During the cellular events of inflammation:
o The antigens travel to nearby lymph node
COMPLEMENT PROTEINS → once in lymph node these antigens bind to the B
● Proteins made by liver cell receptors (IgM and IgG antibodies)
● Constantly circulating int the plasma in the inactive form → this activates the B cells to undergo receptor
● Activated due to mediated endocytosis of antigen-antibody complex
o Chemotaxis into B cell
o ↑vascular permeability → B cell show several expressions
o Fc portion of antibody
● Triggers complement cascade pathways:
o Lectin
 C4 molecules bind directly to mannose
o Classical
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CELLULAR IMMUNITY
(A) B-LYMPHOCYTES
● B-cell expresses
o MHC II molecules on cell membrane
 Which interact with CD4 molecule on T helper
cells
o CD40 molecule
 Which interact with CD 40 ligand of T-helper cells
o Co-stimulation B7 molecules
 Which interact with CD28 on Naïve T helper cells
● The antigen is expressed on the MHC II molecule
o Which interact with T-cell receptor on T-helper cells
(B) CYTOKINES RELEASE
● The B-cell and T-helper cell interaction as listed above
triggers T-helper cells to release cytokines:
o IL-2 → ↑ T cell proliferation
o IL-4 → ↑ B cell Proliferation
o IL-5 → ↑ differentiation of proliferated B cells into
memory B cells and Plasma cells
o IL-5/IL-6 → ↑ Plasma cells to produce antibodies
against antigens on pathogens
T- LYMPHOCYTES
● Antigen presenting cells like macrophages, B-cells and
dendritic cells present antigens on their MHC II molecules
and then present the antigen to T-helper cells
(A) NAÏVE T-HELPER CELLS
● Naïve T helper cells expresses:
o CD4 molecules that binds to the MHC II molecule on
the antigen presenting cells
o T-cell receptor that binds to the antigen expressed
on the MHC II molecule of antigen presenting cells
o CD28 molecules that bind to B7 molecules on
antigen presenting cells
● The antigen presenting cell and T-helper cell interaction
as listed above activates T-helper cells to release the
following cytokines:
o IL-2 → ↑ T cell proliferation
o IL-4 → converts Naïve T cell into TH2 cells (anti-
inflammatory pathway)
o IL-12 → ↑converts Naïve T cells into TH1 cells (pro
inflammatory pathway)
o TGF-beta, IL-1/IL-6/IL-23 → ↑converts Naïve T cells
into TH17 cells
o TGF-beta → converts Naïve T cells into T regulatory
cells
● T regulatory cells → promotes self-tolerance
● Prevents autoantibodies → reducing autoimmune
reactions via TGF-beta and IL-10 release
(1) TH2 Cells
● Fight extracellular pathogens
(i) Stimulate B cell pathway via IL-4/ IL-5
o B cells → Plasma cell → ↑antibody production (IgE)
(ii) Stimulates pathogen killing by activating
eosinophils
(2) TH1 Cell
● Fight intracellular pathogens
(i) Stimulates macrophages via IFN-gamma
o ↑ phagocytosis of pathogens
o ↑ MHC-II expression
IMMUNE SYSTEM OVERVIEW
(ii) Stimulates B cell pathway via IL-2 and IFN-
gamma
o Triggers IgG antibody production from plasma cells
(iii) Stimulates infected cellular killing via NK cells,
cytotoxic T cells
(3) TH17 Cells
● Regulates inflammation and fights extracellular
pathogens
● Regulates Inflammation response (pro and anti-
inflammatory) through use of Neutrophils via IL-1/ IL-21
release
CELL MEDIATED IMMUNITY
(B) CYTOTOXIC T-CELLS
● Kills virus infected cells and neoplastic (cancerous) cells
● When cells are infected by virus or are cancerous this
o Leads to expression of viral antigen or cancer
antigens on MHC-I complex
o MHC-1 complex of infected or cancerous cells interact
with CD8 molecule on cytotoxic T cell
● The cancerous or viral antigen on infected or cancerous
cells interact with T cell receptor on cytotoxic T-cell
o Once cytotoxic T-cells are activated they release
perforins and granzymes
(i) Perforins
o This creates pores in infected or cancerous cells
(ii) Granzymes
o Activates BAX → which removes BCL-2 from
mitochondrial membrane which allows Cytochrome C
to leak into cytoplasm
→ which activate proteolytic enzymes called
caspases → which leads to cell destruction
(apoptosis)
III) NATURAL KILLER CELLS
● It is not a part of the adaptive immunity, only the
mechanism of action is very similar to cytotoxic T-
cells
● They are a part of innate immune system
● NK cells are large agranular lymphocytes
● The activated natural killer cells release Perforins and
Granzymes which trigger apoptosis of viral infected cells
● They can kill by 3 ways:
(1) Absent MHC I molecule expressed on the surface
● All nucleated cells must have MHC I molecule expressed
on the surface
● If a viral pathogen infects tissue cells → virus induces
abnormal MHC I complex or inhibit MHC I formation
● This foreign MHC I or Absent MHC I due to viral infection
→ activates natural killer cells
(2) Different type of MHC I expressed on the surface
(MICA)
● MICA doesn’t contain beta 2 molecule
● Structure of MHC I molecule contains the
o Alpha 1, alpha 2, alpha 3 and beta 2 molecule
● This foreign MHC I like molecule activates natural killer
cells
(3) Through IgG mechanism
● 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→ the
IMMUNOLOGY: Note #1. 3 of 7
 activated natural killer cells then release Perforins and o Myasthenia gravis
Granzymes which trigger apoptosis of viral infected cell o Addison's disease’
o Graves’ disease
(iii) HLA-B27
o Remember: PAIR
IV) MAJOR HISTOCOMPATIBILITY COMPLEXES o Psoriatic arthritis
o Ankylosing spondylitis
● Major histocompatibility complex (MHC) are groups of
o IBD arthritis
genes that code for protein found on the surface of cells
o Reactive arthritis (Reiter’s syndrome)
that help the immune system recognize foreign
substances (iv) HLA-C

(A) MHC-I o Remember: sCaly lesions

o Psoriasis
(1) Structure
(B) MHC-II
(i) HLA-A, HLA-B, HLA-C genes
(1) Structure
o Code for MHC-I peptides
o MHC-1 proteins are broken down into smaller (i) HLA-DP, HLA-DQ, HLA-DR genes
peptides by proteasomes in the cytoplasm then
o Code for MHC-II
transported into the rough endoplasmic reticulum via
o MHC-II peptides are expressed on antigen presenting
a TAP protein
cells like macrophages, dendritic cells and B-cells
o → Then MHC- I peptides are assembled in the Rough
endoplasmic reticulum of nucleated cells (ii) Two polypeptide chains
o → MHC-I proteins are then expressed on all
nucleated cell membranes o MHC-II peptides are made of two polypeptide chains
(long and short chain) of same length
(ii) Two polypeptide chains  Contains alpha chains (alpha-1, alpha-2)
o MHC-I peptides are made of two polypeptide chains  Contains beta chains (beta-1, beta-2)
(long and short chain) of different length
 Long chain
• Contains alpha chains (alpha-1, alpha-2,
alpha-3)
 Short chain
• Contains beta-2 microglobulin chain

Figure 4. MHC-II Structure [Microbeonline]

(2) Function
● When antigen presenting cells phagocytose a pathogen
o It forms a phagosome → combines with lysosomes →
Figure 3. MHC- I structures [Microbeonline] forming a phagolysosome
(2) Function → which break down pathogen leaving small pieces
of pathogen peptides
● When nucleated cells are infected by a viral pathogen or o Simultaneously the HLA-DP/DQ/DR genes increase
become cancerous they express a piece of that viral expression of MHC-II peptides
pathogen or abnormal protein (cancer cells) on the o MHC-II peptides are packaged by the golgi into
MHC-I complex vesicles which combine with the vesicle containing
● Cytotoxic T-cells: the remaining pathogen peptides
o Have a TCR that recognizes the abnormal antigen on o The MHC-II complex expresses a pathogen peptide
the MHC-I complex on the MHC-II complex
o Have a CD8 that recognizes the MHC-I complex on o A vesicle containing both the MHC-II complex with the
the nucleated cell pathogen peptide on its surface are transported to the
● Once this interaction occurs cytotoxic T-cells release antigen presenting cells membrane
perforins and granzymes → this triggers apoptosis of viral o Once on the membrane the antigen presenting cell
infected or cancerous cells interacts with a T-helper cell (CD4)
 The TCR of the T-helper cell interacts with the
(3) Clinical significance pathogen’s peptide on the MHC-II complex
● Mutations or alterations in the HLA genes can precipitate  The CD4 protein on T-cell interacts with the MHC-
autoimmune diseases II complex on antigen presenting cells
→This activates the T-helper cell which triggers
(i) HLA-A3 the release of various cytokines
o Remember: HA3mochromatosis
o Hemochromatosis
(ii) HLA-B8
o Remember: MAG

4 of 7 IMMUNOLOGY: Note #1. IMMUNE SYSTEM OVERVIEW

 Figure 5. Function of MHC-II [Microbenotes]

(3) Clinical significance

● Mutations or alterations in the HLA genes can precipitate
autoimmune diseases
(i) HLA-DR2
o Remember: “Sell Me Good Hay”
o SLE Figure 6. Forms of chemical signaling [BioLibretexts]
o Multiple Sclerosis
o Good pasture syndrome
o Hay fever (B) FUNCTIONAL CLASSIFICATION

(ii) HLA-DR3 (i) Proinflammatory cytokines

o Remember: “Dr Susy Goes Home” o They ↑immune response by

o Diabetes Mellitus Type I  ↑ fever
o SLE  ↑ inflammation
o Graves diseases  ↑ tissue injury
o Hashimoto's thyroiditis o These cytokines are most commonly produced by
TH1 cells
(iii) HLA-DR4 o Most common cytokines
o Remember: RAD  IL-1
o Rheumatoid arthritis (most important)  IL-6
o Addison's Disease  IL-8
o Diabetes Mellitus type I  TNF-alpha
 IFN-gamma
(iv) HLA-DR5
(ii) Anti-inflammatory cytokines
o Hashimoto's thyroiditis
o They ↓ immune response by
(v) HLA-DQ2/8  ↓ proinflammatory cytokine release
o Remember: “you 8 2 much gluten at Dairy Queen  Blocking the binding of proinflammatory cytokines
(DQ)” to other immune cells that will ↑immune response
o Gluten sensitive enteropathy also known as Celiac o These cytokines are most commonly produced by
disease TH2 cells
o Most common cytokines
V) CYTOKINES  IL-4
 IL-10
(A) GENERAL FUNCTIONS  TGF-beta
● Proteins produced by immune cells in response to injury,
infection and ischemia
o Modulate the activity of our immune system
o ↑ inflammatory response
o ↑cellular proliferation and differentiation
● These cytokines can act on target cells in three fashions
(i) Autocrine
o Cell secretes cytokine
o → Cytokine acts on the cell that secreted it
(ii) Paracrine
o Cell secretes cytokine
o → Cytokine acts on a cell nearby
(iii) Endocrine
o Cell secretes cytokine
→ Cytokine travels a farther distance to another cell

Figure 7. Different cytokines [AssayGenie]

IMMUNE SYSTEM OVERVIEW IMMUNOLOGY: Note #1. 5 of 7

 VI) INTERLEUKINS (B) CLINICAL SIGNIFICANCE
● TNF inhibitors (infliximab) are used in diseases with
● Made by macrophages
chronic inflammation such as Crohn's disease
o IL-1, IL-6, IL-8, IL-12
● Made by T-cells VIII) TRANSFORMING GROWTH FACTORS (TGF)
o IL-2 and IL-3
● TGF-beta inhibits inflammatory processes by
(A) FUNCTIONS o Inhibiting a very powerful proinflammatory enzymes
● IL-1 called macrophage proteases
o Stimulates, fever, edema ● Stimulates plasma cells to make IgA antibodies
o Stimulate WBC adhesion and migration through the ● Stimulates tissue growth and repair
expression of adhesion molecules on endothelial cells
● IL-2 and IL-4
o Stimulates differentiation of T-cells → TH2 cells
● IL-4
o Stimulates plasma cells to make IgE & IgG antibodies
● IL-5
o Stimulates plasma cells to make IgA antibodies
● IL-6
o Stimulates synthesis of acute phase reactant proteins
like CRP and Fibrinogen
● IL-8
o Stimulates Neutrophil chemotaxis
● IL-10
o The most important anti-inflammatory cytokine
● IL-12
o Stimulates differentiation of T-cells → TH1 cells

(B) CLINICAL SIGNIFICANCE

(i) Rheumatoid arthritis
o There is ↑IL-1 production so we use a drug called
Anakinra which blocks the effect of IL-1 and its
inflammatory effect on joints
(ii) Transplant rejection
o IL-2 antagonists can be used to prevent transplant
rejection
 Particular kidney transplants
(iii) Asthma/dermatitis diseases
o IL-4 antagonists can be used in asthma and atopic
dermatitis related diseases
(iv) Inflammatory disease
o IL-6 antagonists can be used for inflammatory
diseases like Rheumatoid arthritis

VII) TUMOR NECROSIS FACTOR ALPHA

● Produced by macrophages

(A) FUNCTIONS
(i) Stimulates fever
o Activates hypothalamus
 → ↑Body temperature
(ii) Stimulates edema
o Causes vasodilation and ↑ capillary permeability
 → ↑ fluid leakage into tissue spaces
(iii) Increases WBC migration and adhesion
o ↑ expression of adhesion molecules on endothelial
cells
 ↑adhesion
 ↑diapedesis
 ↑chemotaxis
(iv) Stabilizes or maintains granulomas
o Granulomas are a group of macrophages that form a
rim around giant cells in the center with some
surrounding fibrous tissue and fibroblasts

6 of 7 IMMUNOLOGY: Note #1. IMMUNE SYSTEM OVERVIEW

 IX) QUESTIONS Some defects or mutations in components of
innate or adaptive immunity may lead to
Which of the following cytokine is used for the a. Hypersensitivity
treatment of viral hepatitis and multiple sclerosis? b. auto-immune diseases
a. INF-alpha c. immunodeficiency
b. INF-beta d. tolerance
c. INF-gamma
d. TNF CHECK YOUR ANSWERS

Which of the following interleukin is responsible for X) REFERENCES

T cell expansion after antigen recognition?
● Microbe Online MHC1 and 2 [Digital photo].
a. IL-1 https://microbeonline.com/difference-mhc-class-mhc-class-ii-
b. IL-2 proteins/
c. IL-4 ● Lumen Microbiology Course [Digital image]
https://courses.lumenlearning.com/microbiology/chapter/inflammatio
d. IL-5 n-and-fever/
Which of the following class of cytokine receptors ● Soman N Abraham. ResearchGate [digital image] Retrieved
from: https://www.researchgate.net/figure/Local-effect-of-MCs-on-
utilize G-protein coupled receptor for its the-vasculature-during-acute-inflammation-In-this-
downstream function? diagram_fig3_51639881; 2011
a. Chemokines receptor ● Microbe Notes. MHC function [Digital photo].
https://microbenotes.com/major-histocompatibility-complex-ii-
b. Hematopoietic receptor structure-mechanism-and-functions/
c. Interferon receptor ● Bio LibreTexts. Types of chemicals signaling [Digital photo]
d. None of the above https://bio.libretexts.org/Bookshelves/Introductory_and_General_Bio
logy/Book%3A_General_Biology_%28Boundless%29/9%3A_Cell_C
Cytokines regulate the intensity and duration of the ommunication/9.1%3A_Signaling_Molecules_and_Cellular_Recepto
immune response by activating or downregulating rs/9.1B%3A_Forms_of_Signaling
● Assay Genie. Cytokines [Digital photo]
both innate and adaptive immune response. The https://www.assaygenie.com/cytokines-families-functions
mode of action of the cytokine is the followings ● Aun.edu. MCQ Quiz on Immunology [Quiz]
except: http://www.aun.edu.eg/SECI/questions/Clin_pathology_mcq4.pdf
● MCQ on Cytokines, Interferons & Interleukins 2021.cQuiz]
a. Autocrine https://www.medicalbiochemist.com/2019/03/cytokines-mcq.html
b. Paracrine Immunology:
c. Endocrine ● Oxfor University Press. 2016 Playfair & Bancroft: Infection and
Immunity 4e [Quiz]
d. Cell-autonomous https://global.oup.com/uk/orc/biosciences/immunol/playfair4e/stude
Granulomas formed in response to infection are nt/mcqs/ch20/
● Le T, Bhushan V, Sochat M, Chavda Y, Zureick A. First Aid for
a. Enriched in neutrophils the USMLE Step 1 2018. New York, NY: McGraw-Hill Medical; 2017
b. Enriched in activated macrophages and T cells ● Marieb EN, Hoehn K. Anatomy & Physiology. Hoboken, NJ:
c. Mostly produced in response to viral infections Pearson; 2020.
● Boron WF, Boulpaep EL. Medical Physiology.; 2017.
d. Mostly produced in response to encapsulated ● Urry LA, Cain ML, Wasserman SA, Minorsky PV, Orr RB,
bacteria Campbell NA. Campbell Biology. New York, NY: Pearson; 2020.
● Jameson JL, Fauci AS, Kasper DL, Hauser SL, Longo DL,
Question CD4+ T cells differentiate into different Loscalzo J. Harrison's Principles of Internal Medicine. New York
functional subsets including etc.: McGraw-Hill Education; 2018.
a. Th1 cells secreting IL-4 to activate macrophages ● lberts B, Johnson A, Lewis J, Raff M, Roberts K, Walter P .
Molecular Biology of the Cell. New York, NY: Garland Science;
b. Th2 cells making IL-5 and IL-13 to kill viruses 2002
c. Th17 cells to promote recruitment of neutrophils ● Murphy K, Weaver C. Janeway's Immunobiology. Garland
d. Polyfunctional T cells that secrete IFNγ, IL-4 and IL- Science; 2016
● Doan T, Melvold R, Viselli S, Waltenbaugh C. Immunology.
17 Lippincott Williams & Wilkins; 2012
Cytotoxic T cells which kill their targets ● Levinson W. Review of Medical Microbiology and Immunology.
Lange; 2012
a. Are mostly CD4+
b. Act via perforin and granzyme B
c. Recognize glycolipids in the context of MHC class-I
molecules
d. Also secrete IL-4 and IL-5
Macrophage activation to kill intracellular pathogens
is primarily mediated by
a. IL-2
b. IFNγ
c. GM-CSF
d. IL-12
All of the following are autoimmune disorders
except
a. Graves’ disease
b. SCID
c. Rheumatoid arthritis
d. Addison’s disease
Rheumatoid arthritis mostly occurs in individuals
carrying
a. HLA-DR4 gene (HLA-human leucocyte antigen)
b. HLA-DR1 gene
c. HLA-DR3 gene
d. All of the above

IMMUNE SYSTEM OVERVIEW IMMUNOLOGY: Note #1. 7 of 7