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RUSVM Immunology > Inflammation + Complement > Flashcards

Inflammation + Complement Flashcards

1
Q

What are the effector functions of NK cells?

A
  • lysis of abnormal cells
  • activation of macrophages through cytokine secretion
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2
Q

What are NK cell cytotoxicity mechanisms?

A
  • perforin-dependent mechanism
  • CD95/CD95L (Fas/FasL) mechanism
  • CD16 killing pathway (ADCC)
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3
Q

During perforin-dependent mechanism the NK cell releases perforin from its granules which _______________ called perforin channels.

Later ___________, NK-lysis (granzymes), and __________ are released from cytotoxic granules and passed through the perforin channels, inducing apoptosis of the cell

A
  • creates a lesion
  • granulysin
  • fragmentin (protease)
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4
Q

NK cells normally express CD95L (FasL) on the cell surface, which binds to ______ expressed on target cells, inducing ________

A
  • CD95 (Fas)
  • apoptosis
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5
Q

NK cells can recognize targets through a ____________ using CD16, a _________ receptor.

How does this pathway work? What is its other name?

A
  • antibody dependent pathway
  • Fc (FcyIII)
  • antibodies bind to an antigen on infected cell, NK cells bind to antibodies via CD16 leading to NK cell cytotoxicity
  • ADCC (antibody-dependent cellular cytotoxicty)
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6
Q

T/F: NK cell target recognition through CD16 will only occur when antibodies are present

A
  • true
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7
Q

NK cells are activated by cytokines such as:

A
  • IL-1, IL-2, IL-12, IL-15, IL-18, IL-21, type I + II IFNs
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8
Q

Treatment of isolated NK cells in vitro turns them into __________ with increased cytotoxic ability, which have potential in immunotherapy of tumors

A
  • lymphokine activated killer cells (LAK)
  • some viruses inhibit NK cell cytotoxicity
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9
Q

NKT cells are of _________ origin, with similar properties to NK cells and T lymphocytes. Their specificity is directed against ________ pathogens. They make up 0.5-1% of peripheral blood mononuclear cells

A
  • thymic
  • very few
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10
Q

NKT cells express ____________ TCR, as well as NK1.1 and other KLR receptors.

Mostly they are _______, but can be double negative (CD4-/CD8-).

NKT cells recognize __________

A
  • invariant a/B
  • CD4+
  • glycolipid antigens on bacteria
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11
Q

NKT cells are activated by ______, do not develop into memory cells, and serve to link the T cell system and NK cells.

They play a role in allergies, ___________, autoimmunity,and antimicrobial immunity

A
  • IL-15
  • antitumor immunity
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12
Q

T/F: NK DCs are NK cells with dendritic properties present in the spleen, liver, lymph nodes, and thymus

A
  • false; DCs with NK cell properties
  • NK DCs express NK1.1 and CD11c markers
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13
Q

NK DCs spontaneously _______ tumor cells, present antigens to _________, and produce large amounts of ________ through TLR9 (CpG) stimulation.

A
  • lyse
  • naive T cells
  • IFNy
  • ** link innate and adaptive immunity
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14
Q

Define inflammation

A
  • defense reaction of living tissue against damage, aimed at removing the cause of injury and repairing the tissue.
  • plays a integral role in both innate and adaptive immunity
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15
Q

T/F: inflammation can be either acute or chronic

A
  • true
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16
Q

__________ inflammation fights the early stages of infection and prepares the process that leads to tissue repair

A
  • acute
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17
Q

Chronic inflammation is characterized by:

A
  • dominating presence of macrophages in the injured tissue
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18
Q

What are the exogenous causes of inflammation?

A
  • physical agents
    • mechanical: fractures, foreign objects, sand, etc.
    • thermal: burns, freezing
  • chemical agents: toxic gases, acids, bases
  • **biological agents: bacteria, viruses, parasites, fungi
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19
Q

What are the endogenous causes of inflammation?

A
  • circulation disorders: thrombosis, infarction, hemorrhage
  • metabolic products: uric acid, urea
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20
Q

What are the hallmark signs of of acute inflammation?

A
  • heat
  • redness
  • swelling
  • pain
  • loss of function
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21
Q

The signs of inflammation develop as below:

  • after injury, _________ occurs leading to rise in blood flow raising the temperature (heat)
  • large volume of blood in the area causes __________
  • vascular permeability increases leading to leakage of fluids resulting in ___________
  • within hours leukocytes adhere to the endothelium in the injured area leading to ___________
  • the leukocytes _________ invading pathogens and release mediators that further contribute to inflammation, and some induce pain
  • injured tissue is eliminated from normal function
A
  • vasodilation
  • hyperaemia (redness)
  • edema (swelling)
  • phagocytose
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22
Q

What are the mediators of inflammation?

A
  • pro-inflammatory cytokines
  • complement components
  • prostaglandins
  • leukotrienes
  • vasoactive amines (histamine, serotonin)
  • platelet-activating factor (PAF)
  • plasma proteins
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23
Q

__________ and _________ induce fever and stress hormone production (norepinephrine, vasopressin, activation of RAAS); as well as induce synthesis of IL-,IL-8,and interferon gamma (IFNy)

A
  • tumor necrosis factor alpha (TNFa) + interleukin 1 (IL-1)
  • (pro-inflammatory cytokines)
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24
Q

________ stimulates release of acute-phase proteins such as C-reactive protein (CRP)

A
  • IL-6
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25
Q

Pro-inflammatory cytokines activate the___________, release of nitric oxide, platelet-activating factor, ___________, and ____________.

A
  • coagulation cascade
  • prostaglandins
  • leukotrienes
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26
Q

IL-1, IL-6, and IL-8 promote ________, induce _________ of granulocytes, and ____________ of neutrophils

A
  • chemotaxis
  • extravasation
  • degranulation
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27
Q

The complement components of inflammation C3a andC5a increase ______________ and stimulate __________ of neutrophils, eosinophils, and monocytes

A
  • vascular permeability
  • chemotaxis
28
Q

_________ contribute to vasodilation, capillary permeability, pain and fever during inflammation.

A
  • prostaglandins
  • can lower blood pressure
29
Q

Stable prostaglandins (PGE1 + PGE2) support the effects of _________ and other inflammatory mediators

Prostaglandin _____________ promotes platelet aggregation and vasoconstriction

A
  • histamine
  • thromboxane A2
30
Q

Leukotrienes are eicosanoid inflammatory mediators produced in leukocytes by oxidation of arachidonic acid.

LTC4, LTD4, and LTE4 are slow-acting substances of anaphylaxis (SRS-A) that induce ___________

LTB4 is a ______________

A
  • smooth muscle contraction
  • chemoattractant of neutrophils
31
Q

______________ are found in platelets, basophils, and mast cells, and cause dilation + increased permeability of capillaries

A
  • vasoactive amines (histamine, serotonin)
  • act through HI (histamine) and 5-HT (serotonin) receptors
32
Q

Platelet-activating factor (PAF) is generated from a lipid complex stored in cell membranes. It induces _________, activates neutrophils, is a _____________ chemoattractant, and contributes t efflux of plasma proteins leading to _________.

A
  • platelet aggregation
  • eosinophil
  • edema
33
Q

Plasma proteases, like __________, increase capillary permeability and pain, as well as produce fibrin peptides

A
  • kinins
34
Q

What are the 2 stages of inflammation?

A
  • vascular + cellular
35
Q

T/: the phases of the vascular stage are 1. vasoconstriction, 2. passive vasodilation, and 3. active vasodilation

A
  • false; vasoconstriction, active, passive
  • vasoconstriction: 30s after injury, lasts only a couple minutes
  • active vasodilation: increase in blood flow, active hypermedia, increased cellular metabolism
  • passive vasodilation: vessels stop reacting to stimuli,increase in permeability causes swelling, pain, impaired function
36
Q

The cellular stage of inflammation is marked by movement of _________ into the area of injury, the sequence of events includes chemotaxis, ________, migration, and phagocytosis.

A
  • leukocytes (mainly granulocytes + monocytes)
  • rolling (leukocytes slow down/express adhesion molecules)
37
Q

T/F: the first cells to arrive at the site of infection are cells of adaptive immunity

A
  • false; innate immunity (granulocytes, neutrophils, NK)
38
Q

In order for cells of the immune system to participate in inflammatory response they must use ___________ to migrate

A
  • cell adhesion molecules (CAM)
39
Q

T/F: both the endothelium and leukocytes express CAM, allowing extravasation of leukocytes rom blood vessels into tissues or lymph nodes via adhesion to the endothelium

A
  • true.
  • most CAM are constitutively expressed, some are expressed depending on local conditions.
  • some allow leukocyte-leukocyte interaction
40
Q

What are the 4 families of proteins that make up CAMs?

A
  • selectins, mucins, integrins, Ig-superfamily CAM
41
Q

Selectins are membrane glycoproteins containing extracellular lectin domains that bind _________ on mucin-like molecules.

The most important selectins are selectin ____, _____, ____

A
  • carbohydrate moieties
  • selectin E, L, and P (CD62E, CD62L, CD62P)
42
Q

T/F: selectin P is expressed on leukocytes, selectin L and E are expressed on the endothelium during inflammation

A
  • false; L: leukocytes, P+E: endothelium
  • P: contained in granules in endothelial cells, released when granules fuse with cell membrane
  • E: synthesized de novo following stimulation
43
Q

T/F: mucins are responsible for leukocyte interaction with the endothelium during the initial vascular phase of inflammation

A
  • false; selectins
44
Q

A group of heavily glycosylated, serine- and threonine-rich proteins that bind to selectins:

A
  • mucins
  • ex: CD34 or GlyCAM-1 on endothelial cells binds to CD62Lon leukocytes
  • ex: PSGL-1 on neutrophils binds to selectin E + P on endothelial cells
45
Q

_________ are heterodimeric proteins consisting of a and B chains that are covalently joined at the cell surface, forming a binding site to which the Ig superfamily domains bind

A
  • integrins
  • divided into subgroups according to type of B chain expressed (B1 - B7)
46
Q

Leukocyte express integrins with ______ chain.

Deficiency in this integrin leads to immunodeficiency called leukocyte adhesion deficiency (LAD), an autosomal recessive disorder manifested by _______________ because neutrophils are unable to extravasate

A
  • B2 (CD18)
  • recurrent bacteria infections
47
Q

Ig-superfamily CAMs contain ________________ domains and __________ domains. Important representatives are:

A
  • immunoglobulin-like domains
  • fibronectin domains
  • ICAM-1 (CD154), ICAM-2 (CD102), ICAM-3 (CD50) and VCAM (CD106)
48
Q

T/F; usually selectins bind to integrins and me in-like cams band to Ig-superfamily cams

A
  • false: selectins to mucin-like cams, Ig-superfamily CAMs to integrins
49
Q

Other CAMs have structures with features of both mucins and Ig-superfamily, allowing binding to both ___________________.

A example of this is __________, responsible for migration of leukocytes to mucosa

A
  • Ig-like and mucin domains
  • MAdCAM-1 (binds a4B7 (L-PAM) through Ig-like domain and CD62L through mucin domain)
50
Q

During initiation of inflammation, cytokines and other mediators of inflammation stimulate endothelial cells leading to increased CAM expression. This is called _________________.

A
  • endothelial cell activation
51
Q

What are the 4 phases of extravasation of leukocytes?

A
  • rolling: leukocytes loosely bind to selectin E +P on endothelial cells, slowing down and rolling on endothelium
  • activation: increase in cytokine, specifically chemokine secretion, increases chemokine receptor expression on leukocytes leading to activation
  • adhesion (strict):citi action produces conformational changes allowing integrins on leukocytes to bind firmly to endothelium
  • transendothelial migration: leukocytes squeeze between neighboring endothelial cells and pass into inflamed tissue, using homotypic bonding of platelet-endothelial-cell adhesion molecule 1 (PECAM-11 (CD131)) on the endothelium (self-to-self binding)
52
Q

T/F: Neutrophils are among the first cells to arrive at the site of inflammation and cannot bind to endothelial cells under normal circumstances

A
  • true; without inflammation there is no expression of selectin E, P,and other CAMs n endothelium
53
Q

___________ and mucin PSGL-1 are responsible for rolling of neutrophils

A
  • selectin L
54
Q

IL-8 and IP-1B are responsible for ___________ of neutrophils, which also leads to increased expression of ICAM on the endothelium and __________ on neutrophils, leading to firm adhesion and finally ___________

A
  • activation
  • CD11a/CD18, C11b/CD18 (LFA-1 and MAC-1)
    -diapedesis

-chemokine gradient then leads neutrophils to focal point of inflammation

55
Q

Monocytes arrive slightly late a site of inflammation because high expression of _______________ is only possible after activation stage

A
  • VCAM-1 and ICAM-1
  • only a small subset of monocytes can extravasate under normal circumstances to replenish tissue macrophages and DCs, homeostatic migration regulated by CXCL14
56
Q

In monocyte migration: ______ is responsible for rolling, ______ for activation, _______ for diapedesis, and complement receptors such as CR3/CR4, bacterial peptides participate in extravasation into inflamed tissue

A
  • CD62L
  • MCP-1
  • PECAM-1
57
Q

T/F: lymphocytes are continually circulating between blood and lymphatic tissues

A
  • true, similar extravasation mechanism to neutrophils, pass through post capillary venules (high endothelial venules - HEV)
58
Q

Activation of lymphocytes in HEVs prior to extravasation is mediated by chemokines __________

A
  • CCL19, CCL21, and CXCL12
59
Q

Under optimal conditions, inflammatory response remains localized, but some cases can result in systemic manifestations such as:

A
  • acute phase response
  • alterations in WBC count (leukocytosis or leukopenia)
  • high fever
  • sepsis and septic shock (systemic inflammatory response)
60
Q

Acute phase response refers to ____________ , most of which are synthesized in liver after induction by pro-inflammatory cytokines

A
  • changes in serum proteins
  • acute phase response proteins (APP) - concentrations that change
  • ex: complement system proteins, C-reactive proteins (CRP) - part of innate response
61
Q

T/F: C-reactive proteins belong to pentraxins (pentameric proteins), and are a APP that promote uptake by phagocytes and activate complement mediated attack when bound to microbes

A
  • true;
  • ligands are pneumococcal polysaccharides and phosphorylcholine
62
Q

T/F: mannose-binding lectin is a APRP that recognizes mannose on vertebrate cells and not microbes

A
  • false; microbes and not vertebrate cells
63
Q

What are secondary systemic effects of inflammation?

A
  • loss of appetite
  • altered sleep patterns
  • lethargy
  • muscular wasting (cachexia)
  • metabolic acidosis (lowered blood pH)
64
Q

T/F: when no longer needed, inflammatory response passively ends

A
  • false; must be actively terminated to prevent damages
65
Q

What are inflammation termination mechanisms?

A
  • short half-life of inflammatory mediators in vivo
  • production/release of transforming growth factor (TGF) beta from macrophages
  • IL-4 + IL-10 induce down-regulation of TNFa,IL-1,IL-6, and IL-8
  • downregulation of pro-inflammatory molecules like leukotrienes
  • up-regulation of anti-inflammatory molecules (ex: interleukin 1 receptor agonist or soluble tumor necrosis factor receptor)
  • apoptosis of pro-inflammatory cells
  • down-regulation of receptor activity by high concentration of ligands
66
Q

At end stages of inflammation, granulocytes promote _______________, which initiate the termination sequence. This cease neutrophil recruitment an apoptosis is engaged.

_______ and ________ synthesized from omega-3 polyunsaturated fatty aids shorten neutrophil infiltration by initiating apoptosis

Anti inflammatory process ends with___________

A
  • arachidonic acid-derived lipotoxins
  • resolvins + protectins
  • departure of macrophages through lymphatics
67
Q

What are outcomes of inflammation?

A
  • resolution: complete restoration
  • fibrosis: formation of scar tissue, functional impairment
  • abscess formation
  • chronic inflammation: dominating presence of macrophages, tissue destruction

RUSVM Immunology (3 decks)

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