Module 6A & 6B - Immunology Flashcards
1
Q
Immun/o
A
Exempt/Free From
2
Q
Nat/o
A
Born
3
Q
Medi/o
A
Middle
4
Q
Complet/o
A
To fill up
5
Q
Opson/o
A
Food/Sauce
6
Q
Cyt/o
A
Cell
7
Q
Gland/o
A
Gland/Secreting organ
8
Q
Hist/o
A
Tissue
9
Q
Amin/o
A
Amine
10
Q
Ped/o
A
Foot/To Walk
11
Q
Erythr/o
A
Red
12
Q
Pyr/o
A
Fire/Heat
13
Q
Humor/o
A
Bodily Fluids
14
Q
Top/o
A
Place/Location
15
Q
Agglutin/o
A
Glue/Stick together
16
Q
In-
A
In/Into
17
Q
Prosta-
A
Prostate
18
Q
Brady-
A
Slow
19
Q
Dia-
A
Through/Across
20
Q
Anti-
A
Against/Opposite
21
Q
Epi-
A
Upon/Over/Above
22
Q
-ator
A
One who does/ An agent that performs an action
23
Q
-ment
A
Rest/Action
24
Q
-in
A
Denote protein or other compound
25
-esis
Process or State of
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-ema
Condition/State of
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-gen
Producing
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-al
Pertaining to
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-tion
Act or/ State of
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Cyto-
From the Greek word kytos- meaning cavity or cell
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Kin-
From the Greek word kinesis, meaning movement
The term cytokine combines these elements to describe proteins involved in cell signaling and movement.
Cytokines are small secreted proteins that play
crucial roles in cell-to-cell communication, particularly in immune responses
and inflammation
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What is the first line of defense that is nonspecific? Innate or Adaptive
Innate
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What is the secondary line of defense that is specific? Innate or Adaptive
Adaptive
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What is the status at time of birth? Innate vs Adaptive
Innate
Ready and functional at birth
Adaptive
Ready to develop in response to encounters with microbes
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What time does it become active? Innate vs Adaptive
Innate: Minutes
Adaptive: Days
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Which one of the body’s defense has immunologic memory? Innate or Adaptive
Adaptive
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What are the major components of innate immunity?
• Passive barriers:
- Physical barriers
- Chemical barriers
- Microbiome
• Complement
• Inflammation
• Phagocytosis
• Non-phagocytic killing
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What are the major components of adaptive immunity?
• Cell-mediated immune response (cytotoxic)
• Humoral immune response (antibodies)
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What is the function of cellular barriers?
Example of this?
Cellular barriers
-Deny entry to pathogens
- Example: Skin, mucous membranes, endothelial cells
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What is the function of mechanical defenses?
Example of this?
Mechanical defense:
- Remove pathogens from potential sites of infections
- Examples: Shedding of skin cells, mucociliary sweeping, peristalsis, flushing action of urine and tears
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What is the function of microbiome?
Example of this?
Microbiome:
- Complete with pathogens for cellular binding sites and nutrients
- Examples: Resident bacteria of the skin, upper respiratory tract, gastrointestinal tract, and genitourinary tract
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What is the function of physical barriers? What are the examples of physical barriers? What are the tight junctions between cells?
• Prevent pathogens from reaching
susceptible tissues
• Skin, mucous membranes, epithelial cells
• Tight junctions between cells:
- Complementary proteins in cell membrane of
adjacent cells
- Most commonly: One is a glycoprotein and the
complementary protein a lectin with a specific
binding site for the oligosaccharide of the
glycoprotein
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What are some examples of chemical barriers in the body’s defense?
• Sebaceous glands in dermis - sebum (oil) - seals hair follicle pore and sweat glands
• Lipases from skin microbiome bacteria leads to release of fatty
acids from sebum oil - mildly acid environment adverse for many
pathogens
• Salt from sweat also produces adverse growth conditions
• Stomach acid is detrimental for many microorganisms
• Lysozyme in tears and mucus in esophagus breaks down peptidoglycan in bacterial cell wall
• Antimicrobial peptides: class of nonspecific cell-derived mediators with broad-spectrum antimicrobial properties
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What are the 3 major groups of plasma protein mediators
1. Acute-phase proteins
2. Complement proteins
3. Cytokines
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What are some characteristics of acute-phase proteins? Where is produced? Examples?
• Class of antimicrobial mediators
• Primarily produced in the liver
• Examples of acute-phase proteins:
C-reactive protein
Serum amyloid A
- Coats bacteria (opsonization) - phagocytosis
Ferritin and Transferrin
- Bind and sequester iron - inhibits (or slows down) growth
Fibrinogen
- Involved in blood clot formation - traps bacterial pathogens
Mannose-binding lectin
- Activation of complement cascade (‘lectin pathway’)
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What is the complement system?
A group of over 30 plasma proteins that enhance innate immunity and connect innate and adaptive immune responses.
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How are complement proteins activated?
Some complement proteins circulate in an inactive form and are activated when the cascade is triggered.
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What are the three pathways that activate the complement system?
The classical pathway (antibody-mediated), the lectin pathway (triggered by MBL), and the alternative pathway (directly activated by pathogen surfaces).
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How does the complement system enhance pathogen clearance?
It helps with opsonization, directly attacks pathogens, and promotes immune cell activation.
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What are the 3 ways of complement activation?
Alternative pathway
Classical pathway
Lectin pathway
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How does alternative pathway get triggered? What does it depend on?
- Presence of invading microbe
- Self-decay if inactive C3; if it does not bind to microbe, C3b gets lysed
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How does classical pathway get triggered? What does it depend on?
- Presence of antibody-antigen complex (immune complex)
- Upregulation of adaptive immunity (humoral immunity)
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How does lectin pathway get triggered? What does it depend on?
- Lectins binding to mannose-containing microbial surface structure
- From liver and other cells and macrophages (involved in inflammation)
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What are the three main outcomes of complement activation?
Inflammation, opsonization, and formation of the membrane attack complex (MAC).
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Which complement proteins are responsible for inflammation?
C3a, C4a, and C5a
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What is the role of C3a, C4a, and C5a in inflammation?
They attract phagocytic cells to the site of infection.
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Which complement protein is responsible for opsonization?
C3b
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How does C3b contribute to immune defense?
It coats pathogens, making them easier for phagocytic cells to recognize and engulf.
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Which complement protein initiates the formation of the membrane attack complex (MAC)?
C5b, C6, C7, C8
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What is the function of the membrane attack complex (MAC)?
It creates holes in the membranes of target cells, leading to cell lysis.
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How does MAC kill pathogens?
By puncturing holes in their membranes, causing them to lose structural integrity and burst.
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What are interleukins, and what was originally believed about their function?
Interleukins were originally thought to only mediate communication between white blood cells, but they can also come from and affect other cell types, playing roles beyond immune function.
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What are chemokines?
Chemokines are chemotactic factors that recruit specific types of white blood cells to sites of infection or injury.
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What are the main functions of the complement system?
Marking cells for lysis, enhancing phagocytosis (opsonization), attacking viral envelopes, and attracting more phagocytes.
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What are the main triggers of complement activation?
The presence of pathogens, antibody binding (classical pathway), mannose-binding lectin (lectin pathway), and direct recognition of pathogen surfaces (alternative pathway).
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What are the key outcomes of complement activation?
Inflammation, opsonization, and formation of the membrane attack complex (MAC), leading to pathogen destruction.
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How does the complement system contribute to opsonization?
Complement proteins coat pathogens, making them easier for phagocytes to recognize and engulf.
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What effect does complement activation have on phagocytes?
It attracts more phagocytes to the site of infection, enhancing immune response.
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What are cytokines?
Soluble proteins that act as communication signals between immune cells.
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How do cytokines function in the immune system?
They originate from certain cells and bind to receptors on other cells to regulate immune responses.
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What are the three major classes of cytokines?
Interleukins, chemokines, and interferons.
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What is the role of interleukins?
They regulate immune cell growth, differentiation, and activation.
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What is the function of chemokines?
They guide the movement of immune cells to infection or injury sites.
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What do interferons do?
They help defend against viral infections by signaling cells to produce antiviral proteins.
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What are interferons?
Interferons are cytokines released by virus-infected cells that help prevent the spread of infection to neighboring cells.
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What do interferon-α and interferon-β do?
They signal uninfected neighboring cells to inhibit mRNA synthesis, destroy RNA, and reduce protein synthesis, slowing viral replication.
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How do interferon-α and interferon-β affect infected cells?
They promote apoptosis (programmed cell death) in virus-infected cells to limit the spread of infection.
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What is the function of interferon-γ?
It alerts neighboring immune cells to an attack, enhancing the immune response.
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Can interferons cure an infected cell?
No, interferons do not cure infected cells, but they help prevent additional cells from becoming infected, limiting the spread of the virus.
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What is histamine, and where is it derived from?
Histamine is derived from the amino acid histidine and is released by mast cells and basophils.
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What are the effects of histamine?
It leads to vasodilation, contributing to inflammation and hypersensitivity reactions.
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What are eicosanoids, and what are they derived from?
Eicosanoids are signaling molecules derived from the omega-6 fatty acid arachidonic acid.
83
When are eicosanoids released?
They are released by mast cells near damaged cells and by viable damaged cells themselves.
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What are leukotrienes, and how do they function?
Leukotrienes have effects similar to histamine but are stronger, promoting inflammation.
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What are prostaglandins, and what are their effects?
Prostaglandins cause pain, make blood vessels leaky, and promote fever.
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What is bradykinin, and what type of molecule is it?
Bradykinin is a short polypeptide involved in inflammation.
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What are the effects of bradykinin?
It makes blood vessels leaky, allowing leukocytes and fluid to leave the bloodstream, leading to edema (swelling).
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How is bradykinin activated?
It can be activated by the blood clotting cascade or upon contact with foreign surfaces (e.g., metal, glass).
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What is acute inflammation?
A cascade of chemical mediators and cellular responses triggered by cell damage or stress to eliminate pathogens and remove dead or damaged cells.
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What are the main functions of acute inflammation?
Recruitment of cellular defenses, elimination of pathogens, removal of damaged cells, and initiation of repair mechanisms.
91
What can excessive inflammation lead to?
Tissue damage and, in severe cases, death.
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What is chronic inflammation?
Prolonged inflammation lasting longer than several weeks due to various underlying causes.
93
What is the first step in the inflammatory response after a cut?
The cut penetrates the epidermis, allowing bacteria to invade.
94
What happens after bacteria invade a cut?
Damaged cells and mast cells release histamine, prostaglandins, and leukotrienes.
95
What do histamine, prostaglandins, and leukotrienes do in the inflammatory response?
They cause vasodilation and increase blood vessel permeability, leading to redness (erythema) and heat.
96
How do neutrophils and macrophages reach the infection site?
They squeeze through the walls of blood vessels (a process called diapedesis) to reach the damaged tissue.
97
What forms at the site of injury to prevent further infection?
A blood clot forms, helping to seal the wound.
98
What role does bradykinin play in inflammation?
It extends vasodilation, allowing more immune cells to reach the infection site.
99
What happens after more phagocytes arrive at the site of injury?
They engulf and destroy bacteria, helping to clear the infection.
100
What causes pus formation during inflammation?
The accumulation of dead bacteria, damaged tissue, and leukocytes leads to pus formation.
101
How is damaged tissue repaired after inflammation?
Undifferentiated stem cells regenerate tissue, and fibroblasts produce new collagen to restore the extracellular matrix.
102
What happens to the blood clot after tissue repair?
The clot is either absorbed or falls off as healing completes.
103
What is the effect of increased blood vessel permeability during inflammation?
It allows antimicrobial chemicals and clotting proteins to enter damaged tissue but also causes swelling, pressure on nerve endings, and pain.
104
How does acute inflammation differ from systemic inflammation?
Acute inflammation is a local response to infection or injury, while systemic inflammation affects the entire body.
105
What triggers a systemic inflammatory response?
Pyrogens—biomolecules that alter the ‘thermostat’ setting in the hypothalamus—trigger an overall increase in body temperature (fever).
106
What are the effects of increased body temperature during a systemic response?
• Slows bacterial growth by moving the temperature away from optimal growth conditions.
• Enhances iron-sequestration, limiting bacterial access to iron.
• Speeds up phagocytosis, improving immune response.
107
What are the main components involved in opsonization?
Antibodies, C3b, lectins, and C-reactive protein.
108
What are pathogen-associated molecular patterns (PAMPs)?
PAMPs are molecular structures common to many groups of pathogens.
109
Can you give examples of PAMPs?
Peptidoglycan (bacterial cell wall), lipopolysaccharide (outer membrane of Gram-negative bacteria), flagellin (protein in flagella), lipopeptides (common for many bacteria), viral DNA or RNA.
110
What are pattern recognition receptors (PRRs)?
PRRs are receptors, such as toll-like receptors (TLRs), located on the surface of phagocytic cells and in membranes of intracellular compartments that recognize PAMPs.
111
What happens when a PAMP binds to a complementary PRR?
The phagocytic cell becomes activated.
112
What do phagocytic cells contain to recognize pathogens?
Phagocytic cells contain pattern recognition receptors (PRRs) that can recognize various pathogen-associated molecular patterns (PAMPs).
113
Where can pattern recognition receptors (PRRs) be found?
PRRs can be found on the plasma membrane or in internal phagosomes of phagocytic cells.
114
What happens when a pattern recognition receptor (PRR) recognizes a pathogen-associated molecular pattern (PAMP)?
When a PRR recognizes a PAMP, it sends a signal to the nucleus that activates genes involved in phagocytosis, cellular proliferation, production and secretion of antiviral interferons and proinflammatory cytokines, and enhanced intracellular killing.
115
What is the role of phagocytosis in the immune response?
Phagocytosis leads to the degradation of foreign particles, damaged cells, and dead cells into building blocks and waste products. It also removes extracellular pathogens and fragments of pathogens.
116
Which leukocytes are involved in phagocytosis with major activity?
Neutrophils, macrophages, and dendritic cells.
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What is the lifespan and role of neutrophils in inflammation?
Neutrophils (approx. 60% of all leukocytes in blood) have a short lifespan of a few days and are the hallmark leukocyte of acute inflammation.
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What is the lifespan and role of macrophages in inflammation?
Macrophages, derived from monocytes, have a longer lifespan (months or even longer) and are the hallmark immune cell of chronic inflammation.
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Where are dendritic cells derived from, and what is their role?
Dendritic cells are derived from monocytes and are embedded in skin and mucous membranes. They technically perform endocytosis.
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What do phagocytes use to recognize microbial cells?
Phagocytes have specialized toll-like receptors (TLRs), also called pattern recognition receptors (PRRs), to bind distinguishing patterns (PAMPs) on the surface of microbial cells.
121
What happens when a phagocyte binds a microbe with its receptors?
The membrane surface of the phagocyte folds and encapsulates the microbe into a vacuole called a phagosome.
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What role do lysosomes play in phagocytosis?
Lysosomes concentrate digestive chemicals and enzymes, which then fuse with the phagosome to produce a phagolysosome.
123
What occurs within the phagolysosome?
The microbial cell is killed within the phagolysosome, and the digested material is expelled from the cell.
124
What is the role of eosinophils in nonphagocytic killing?
Eosinophils attack parasitic helminths by attaching to their surface and secreting toxins that weaken or kill them. A high eosinophil count (eosinophilia) is indicative of helminthic infection.
125
What is the role of natural killer (NK) lymphocytes in nonphagocytic killing?
NK lymphocytes recognize virus-infected cells and induce them to undergo apoptosis. Their activity is enhanced when the cell-mediated immune response is ramped up.
126
What does a high leukocyte count typically indicate?
A high leukocyte count typically indicates a bacterial infection, due to high neutrophil activity.
127
What does a high lymphocyte count typically indicate?
A high lymphocyte count is indicative of a viral infection.
128
What does a high eosinophil count typically indicate?
A high eosinophil count suggests a parasitic worm infection or an allergic reaction.
129
Where do B lymphocytes mature? Differentiate into?
- From lymphoid stem cells
- Mature in the bone marrow
- Differentiate into
— Plasma cells - antibodies: target extra-cellular pathogens and toxins
—Memory B cells
- Humoral immunity
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Where do T lymphocytes mature? Differentiate into?
- From lymphoid stem cells
- Mature in the thymus
- Differentiate into
— T cells with various regulatory functions (T helper, T regulatory)
— Cytoxic T cells: target intra-cellular pathogens, cancer cells
— Memory T cells
- Humoral and cellular immunity
- Humoral immunity
131
What are antigens?
– Pathogen-specific molecular structures; unique to a specific pathogen
– Play role in stimulating humoral and cellular immunity
Can be:
– Proteins
– Carbohydrates
– Lipids
– Nucleic acids
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What are epitopes antigens?
– Smaller exposed region on surface of an antigen
– A large, complex protein may have hundreds of epitopes
– Each unique epitope can only be bound by a specific antibody
133
What are haptens?
– Small molecules that cannot be antigenic by themselves but as a component of a conjugate
– Not associated with pathogens but responsible for some allergic reactions
– Antibodies produced against the small molecule will bind to free hapten (‘free’ epitope)
134
What is another name for antibodies?
Immunoglobulins
135
What are the direct effects on pathogen/toxin? What are the indirect effects?
Direct effects on pathogen/toxin:
– Neutralization
– Agglutination
Indirect effects onpathogen/toxin:
– Opsonization
– Antibody-dependent cellular cytotoxicity
– Activation of complement: ‘Classical pathway’
136
What is the function of IgG monomer?
Neutralization
Agglutination
Opsonization
Complement activation
Antibody-dependent
Cytotoxicity
137
What is the function of IgM pentamer?
Neutralization
Agglutination
Opsonization
Complement activation
Monomer from is B-cell receptor
138
What is the function of IgA dimer?
Neutralization and trapping of pathogens in mucus
139
What is the function of IgD monomer?
B-cell receptor
140
What is the function of IgE monomer?
Activation of basophils and mast cells against parasites and allergens
141
What is the Major Histocompatibility complex?
– A group of molecules first identified in graft patients: ‘human leukocyte antigen’ or HLA
– Glycoproteins, found in cytoplasmic membranes
– HLA testing is vital to determine donor and graft recipient compatibility
– In context of immune response, we use ‘MH
142
Where are the MHC I found? What is it major role?
– Found in all nucleated cells (cytoplasmic membrane)
– Internal molecules are partially degraded and presented at the surface of cells
– Plays a major role in self-tolerance
– Immune system is alerted if cell is ‘abnormal’, not healthy
—Intracellular pathogens (especially viruses)
—Tumor cells
143
What is the structure of self-tolerance? What is the function?
– Structure of epitope-binding sites in B and T-cell receptors are randomly formed (randomized amino acid sequence) - some receptors bind to autoantigens (autoimmunity)
– To prevent immune response against autoantigens, body eliminates self-reactive lymphocytes through ‘clonal deletion’ - triggers B- and T-cells that are binding to our own antigens to undergo apoptosis
144
What are Antigen-Presenting Cells (APCs)?
– Macrophages, dendritic cells, B lymphocytes
– Have MHC II (in addition to MHC I)
– Antigen-presentation in lymph nodes
– Upregulation of adaptive immunity
– Macrophages, dendritic cells:
– Part of the innate immune response
– Recognize pathogens through PAMPs
– Phagocytes that ingest and kill pathogens
– B lymphocytes
– Part of the adaptive immune response
– Recognize specific epitopes with B cell receptors (IgD and IgM)
– More on this type of antigen-presentation in the humoral immune response lesson
145
What is another name for cell-mediated immunity? What does it target and eliminate?
– Also called cellular immunity
– Targets and eliminates intracellular pathogens through cytotoxic T cells
146
Helper T cells (Th cells)
What is the surface CD molecules?
What is the activation?
What is the function?
CD4
APCs presenting antigens bound to MHC II
- Orchestrate adaptive immunity
- Activation of macrophages and NK cells
147
Regulatory T cells (Treg cells)
What is the surface CD molecules?
What is the activation?
What is the function?
CD4
APCs presenting antigens bound to MHC II
- Involved in self-tolerance and prevention of autoimmunity
148
Cytotoxic T cells (Tc cells)
What is the surface CD molecules?
What is the activation?
What is the function?
CD8
APCs or infected cells presenting antigens bound to MHC I
- Destroy cells infected with intracellular pathogens
149
What are T cell receptors (TCR)?
– Antigen-binding site is epitope- specific
— Antigen must be bound to MHC I or II
– Estimate: 25 million unique epitope binding sites
—Formed through ‘genetic rearrangement’ (happens while in thymus)
150
What happens during activation/differentiation of helper T cells?
– Also called Th cells and CD4+ lymphocytes
– MHC II presents to T cells that
have CD4 membrane complex
– Successful binding between presented epitope and T cell receptor triggers clonal proliferation and differentiation
151
What are the functions of helper T cells?
Th 1 lymphocytes vs Th 2 lymphocytes
Th 1 Lymphocytes
• Secrete IL-2
• Activation and differentiation of CD8 lymphocytes to form cytotoxic T cells
• Stimulation of macrophages and
neutrophils
• Stimulation of NK cells
Th 2 Lymphocytes
• Secrete IL-4
• Activation and differentiation of B
lymphocytes - antibody production
• Regulate what type of antibody class is produced
152
What is humoral immunity
Immunity mediated by antibodies secreted by highly differentiated B lymphocytes, called plasma cells
153
What happens during B cell production and maturation?
– Derived from lymphoblasts
– Stay in bone marrow for maturation
– Clonal deletion or negative selection eliminates self-reactive B cells
– Final maturation steps happen in spleen: Naïve mature B cells
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