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I&D Flashcards

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1
Q

What are the 4 main immune compartments? Which ones use cytokines and chemokines?

A

Innate: complement, phagocytes
Adaptive: B cells and T cells
Phagocytes and T cells use cytokines and chemokines.

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2
Q

What happens if the complement doest work?

A

Since complements creates opsonization, when it’s defective lots of encapsulated bacteria due to inefficient opsonization and phagocytosis. So we get lots of infection by encapsulated bacteria (like strep)

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3
Q

What is the end result of complement? How does it happen?

A

It’s the landmines of the innate system. After triggering several activation events –> end up in “explosion”. Major role is opsonization (coating of bacteria for phagocytosis) and formation of membrane attack complex (MAC)

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4
Q

What are some unique features of phagocytes? How are they related to T-cells?

A
  1. They move to the site of infection through tissue like marines and they are first deployed to the battle
  2. They eat, digest and present antigens to T-cells, T cells in turn required to have MHC to actually recognize peptides presented
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5
Q

What happens if phagocytes doesnt work? What disease can it cause?

A

Lots of infections by catalase + organisms, soft tissue abscesses, lymphadenitis and poor wound healing. Causes Chronic Granulomatous Disease ( defective NADPH oxidase -important for innate immunity) and unable to kill catalase + bacteria

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6
Q

What is the of of B cells?

A

B cells are like air force: the main role is to deploy a/b(immunoglobulins) that are like cruise missiles. Can deploy at or near site of inflammation or can be distant

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7
Q

What happens if B cells and A/B dont work?

A

Recurrent bacterial sinopulmonary infections

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8
Q

What is the role of T cells? What are the roles of three different types?

A

Known as generals, assassins and psychologists of the immune system

  1. CD4 - helper T cell: directs immune system where to go
  2. CD8 - cytotoxic T cells kill cells infected with intracellular pathogens like viruses, fungi, etc
  3. regulatory T cells control and modulate immune responses - modulates autoimmune and immune system, have to keep cells under control
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9
Q

What if T cells don’t work?

A
  • cant generate effective a/b response
  • severe viral infections (Herpes Simplex virus type 5(CMV) and type 4 (EBV))
  • severe fungal infection
  • autoimmunity
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10
Q

What do we mostly have issues with during one of the compartments absent?

A

Complement - encapsulated bacteria

Phagocytes - Bacteria, Fungi, Molds

B cells - bacteria

T cells - viruses, fungi, bacteria

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11
Q

What are the two goals of micro?

A

see

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12
Q

bacterial envelope: difference for G+ and G- bacteria? Why is this difference in cell wall assembly important?

A

One cell membrane surrounded by a thick cell wall: G+

Additional outer membrane: G-

Important because its an antibiotic target

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13
Q

What does cell envelope structure determine?

A

cell envelope structure Determines the gram stain

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14
Q

What are bacterial appendages and capsules important for?

A

colonization, attachment, movement. Its a part of pathogen factor

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15
Q

What are the 4 appendages in bacteria?

A
  1. flagella -colonize
  2. Pili/fimbriae - attachment are virulence factors
  3. specialized secretion systems-syringes to inject substances into the host
  4. capsules - external mucoid polysaccharide layer avoids immune recognition and phagocytosis
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16
Q

How does mucosal clearance happens? What are some barrier in mucosa?

A

tight junctions and mucus barrier forms a barrier

movement happens with cilia and peristalsis

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17
Q

What bactericidal compounds are present in mucus?

A
  1. Acid in stomach
  2. bile detergents in intestine
  3. antimicrobial peptides and enzymes
  4. IgA
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18
Q

What are the ways pathogens evade mucus clearance?

A
  1. Viruses have specialized molecules that attach to specific host-cell receptors (our body has receptors that help virus-ligand interaction, like sialic acid (for influenza) is a receptor our body has) Note! The physical barrier isn’t compromised. Its just a normal receptor
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19
Q

Whats is the other way other than receptors that pathogens can enter?

A

defective epithelia barrier!

skin defects, anatomic defect (Tracheoesophageal fistula), mucosal defects (chemotherapy causes mucositis)

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20
Q

how do pathogens cross the epithelial barrier?

A

Via target cells involved in immune surveillance

  1. dendritic cells - HIV (macrophages and DC on the surface of the membranes bind viruses and shuttle into lymph nodes
  2. Intestinal M cells - Salmonella
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21
Q

Does infection have to involve invasion?

A

NO. they can attach to cilia and use toxins to cause damage or they can attach and just steal nutrients

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22
Q

what are the 5 ways to avoid immune detection and

A
  1. intracellular invasion
  2. capsules to avoid phagocytosis
  3. antigenic variation
  4. immune modulation (go through)
  5. residence in immune privileged sites (VZV in sensory neurons in dorsal root ganglia and trigeminal ganglia)
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23
Q

How do bacteria and fungi steal nutrients? Whst do thry acquire?

A

using toxins. Micronutrients: iron (essential metal nutrient), sidephores (high-affinity iron chelating compounds), digestive enzymes

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24
Q

What are the three complement systems? What are they activated by?

A
  1. Classical pathway - activated by immune complexes (initiated by binding of an immune complex c1 to ab-ag complexes. Only IgM (mostly) and IgG can activate this complement. IgM>>>IgG3>IgG1>IgG2)
  2. Lectin pathway - activated by Pathogen Oligosaccharides -they recognize specific oligosaccharides (Mannose binding lectin (MBL) recognizes oligosaccharides associated with bacteria, yeast and parasites but DOESNT bind mammalian glycoproteins )
  3. Alternative pathway - activated by pathogen surfaces ( spontaneously activated by contact with various proteins, lipids, carbohydrates structures on pathogens)
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25
What are the 5 major roles of complement?
Regardless of which one of the three pathways to take it forms MAC and attack bacteria. As a side arm it can attract Macrophages, Neutrophils, and activate Mast cells -→ HISTAMINE release 1. **Opsonization**: Most important, binds to surface or encapsulated, slippery, slimy bacteria and provides handles for phagocytes to bind and ingest them 2. **Cytolysis**: Forms MAC and directly destroyes bacteria 3. **Promotes AB production by B cell**s -enhances B cell AB response (Helping AB which are already made do their job) 4. **Chemotaxis** - promotes movement of leukocytes into tissues. Draws innate immune cells to sites of inflammation 5. **Removal of immune complexes and apoptotic cells-**by phagocytosis
26
What is the classical pathway? Which immoglobulins can activate it?
initiated by binding of an immune complex c1 to ab-ag complexes. Only IgM (mostly) and IgG can activate this complement. IgM\>\>\>IgG3\>IgG1\>IgG2
27
How does Lectin pathway gets activated?
Mannose binding lectin (MBL) recognizes oligosaccharides associated with bacteria, yeast and parasites but DOESNT bind mammalian glycoproteins
28
What are the four different steps how the body recognizes and evade pathogens?
Sensor-→ Alarm → Resident → Recruit
29
How does the cell senses the non-self vs self? 2 things + examples
1. **DAMPs**: damage associated molecular patterns: 1. HPS: heat, toxins, oxidants. Reduce denaturation/ enhance renaturation to regain correct tertiary structure 2. HMGB1 released by necrotic cells can mediate inflammation in CNS & peripheral tissues 3. MSU crystals precipitate within joints & soft tissues → inflammation → gout 1. **PAMPs** (pathogen associated molecular patterns)
30
Whats the example of DAMP that we have seen in purine/pyrimidine metabolism?
Excess purine leads to monosodium urate (MSU-one of the examples of DAMPs) which leads to inflammation and Gout.
31
Whats the example of DAMP that we have seen in purine/pyrimidine metabolism?
Excess purine leads to monosodium urate (MSU-one of the examples of DAMPs) which leads to inflammation and Gout.
32
What are PRPs and what is their role in immunity? What are the 5 functions?
They recognize PAMPs. 1. recognize pathogen by specific type 2. Stimulate immune responses of specific types 3. required to stimulate adaptive immune responses to infection and vaccination 4. Activation of specific PRRs is associated with specific diseases 5. Genetic differences in PRR activity predispose people to specific diseases
33
What are the 6 different cell-associated PRPs? And who do they target?
The ones she went over: **RIG-Like receptors (RLRs**) - cytoplasmic on multiple cell types, sense _viruses_ **C-Type Lectin receptors**: targets microbial carbohydrates in _bacterial_, _viral_ and _fungal_ cell membranes
34
What are the important TLR's and what are they targeting and where are they located ?
1. **TLR2**- peptidoglycan (so G+. surprisingly P.gingivalis has it, even though g-) C_ell surface_ 2. **TLR4**- LPS→ G- _Cell surface_ 3. **TLR5** - Flagellin C_ell surface_ 4. **TLR9** - Unmethylated CpG DNA - Endosomal
35
What receptors does our body have to sense pathogens in the cytosol? What do they sense? What do they signal through?
NOD-Like receptors (family of more than 20) Sense cytoplasmic PAMPs and DAMPs (peptidoglycans, flagellin, viral RNA, Fungal hyphae) Signal through “Inflammasomes” → activate caspases→ generate mature IL-1b
36
What are the 4 cell's innate alarm signals? What effect does it reach?
they cause local, regional and systemic effect 1. Cytokines 2. Chemokines 3. Leukotrienes and Prostoglandins 4. Acute phase reactants
37
What are the 3 major inflammatory cytokines?
TNFa IL-1 IL-6
38
What are the local effects for TNFa, IL-1, IL-6. How does TNFa induce the inflammation?
TNFa induces inflamation through NFkB Local effects: 1. activates endothelial cells (to recruit leukocytes) to express selectin ligands, cell adhesion molecules, and chemokines 2. activate resident immune cells 3. stimulate phagocytosis, production of oxidants for microbe killing, and production of prostaglandins
39
What are the 5 systemic effects of TNFa?
1. Act on the hypothalamus as endogenous pyrogens (increases fever) 2. Induce hepatocytes to express acute-phase reactants (C-reactive P, fibrinogen, Complement) 3. TNFa specific:inhibits myocardial contractility and vascular smooth muscle tone→ hypotension 4. TNFa specific: causes intravascular thrombosis 5. TNFa specific: causes wasting of muscle and fat cells -cachexia
40
What are the 2 systemic effects of IL-1 and IL-6?
1. Act on the hypothalamus as endogenous pyrogens (increases fever) 2. Induce hepatocytes to express acute-phase reactants (C-reactive P, fibrinogen, Complement)
41
What is Cachexia and what is it caused by?
weaken muscle tone. Systemic effect of TNFa!
42
What happens if too much cytokines are released (3 things)? Why does it happen (3 reasons)?
What? results in “cytokine storm” and causes systemic inflammatory response syndrome (SIRS): vascular collapse, disseminated intravascular coagulation, severe metabolic disturbances Why? Cytokine storm is caused by bacterial sepsis, toxic shock, large scale lymphocyte activation
43
What are the two types of lipid inflammatory mediators pathways and the mediators? What do they cause? What are they derived from?
1. Cyclooxyrgenase pathway→ Prostaglandins: cause vasodilation/vascular permeability, inflammatory pain, hyperalgesia, Fever 2. Lipoxygenase pathway pathway →Leukotrienes: cause allergic reactions and inflammation
44
What are chemokines? What are their roles?
-large family of small secreted molecules, they are chemotactic cytokines. **Form chemotactic gradients and lead immune cells and WBC to an infection site** they can be presented on the surface if endothelium stimulate leukocyte migration and leukocyte integrins Tell WBC where to go!
45
What are the two types of inflammatory chemokines covered in lecture? What do they recruit?
1. **IL-8 (CXCL8**) -recruits NEUTROPHILS 2. **Monocyte chemoattractant Protein (_MCP-1,_ CCL2**) - recruits monocytes
46
are inflammatory cytokines expressed in normal tissues?
No
47
How are inflammatory chemokines turned on?
By PRR activation and by inflammatory cytokines
48
What are the 4 types of resident innate Immune cells? Why are resident cells important?
Important-they are the first responders when microbes breached the mucosal barrier 1. Mast cells 2. Macrophages 3. dendritic cells 4. Innate-like lymphocytes
49
Where are mast cells located? What do they protect against? How are mast cells get activated?
Mucosal surfaces of the gut, lungs 🫁 , skin, around blood vessels They defend against parasitic infection and in allergic reactions Activation: **IgE** binds and causes mast cells degranulation.
50
What happens after mast cell degranulate?
Activation: **IgE** binds and causes mast cells degranulation. The effects of degranulation: 1. biogenic amines → vasodilation and vascular leak 2. Cytokines → Inflammation 3. Enzymes → Tissue damage Note: our body activates smth that causes tissue damage
51
What are the 4 main functions of Macrophages?
1. Phagocytosis 2. Release cytokines and growth factors for wound healing 3. ROS&NO to kill phagocytosed bacteria 4. Repair damaged tissue by stimulating angiogenesis and fibrosis
52
What are the three steps of phagocytosis?
1. recognition and attachment 2. Engulfment and fusion of phagosome and lysosome 3. Killing and degradation of ingested material (ROS and NO)
53
What is the main role of dendritic cells?
They are AG processing cells They capture and process Antigens, converting proteins to peptides that are presented on MHC molecules recognized by T cells
54
Why is dendritic cells cells sometimes referred as to a bridge between innate and adaptive immunity?
They get activated by PRRs, and cytokines and in turn activate the T cells, B cells, NK cells, macrophages, Interstitial cells
55
What are the first cells to respond during an infection?
Innate like lymphocytes
56
Where are innate like lymphocytes found?
Intestinal mucosa, skin, lungs
57
What are the 5 recruited immune cells?
Neutrophils, Monocytes, NK, Eosinophils, basophils
58
What is the first recruited inflammatory cell to arrive?
Neutrophils. Fastest to arrive, but half life is only 6-8 hours. Most active in extra cellular bacterial infection
59
What are neutrophils mediated by?
Mediated by ROS and phagocytosis
60
What is the main job of neutrophils?
Production of anti microbial peptides- human neutrophil peptides (HNPs), alpha defensins
61
What are the most long lasting cells out of recruited inflammatory cells?
Monocytes. They can differentiate into Macrophages
62
What are monocytes mostly effective against?
I travel lunar bacteria And viruses!
63
What are the 3 jobs of monocytes?
- Eat dead and dying cells -responsible for cleanup - Produce large amounts of cytokines and chemokines to promote further inflammation - When infection resolves they produce proteases and growth factors to meditate tissue repair
64
What is the job of NK cells and how do they accomplish it?
Kill infected cells and activate macrophages to destroy phagocytosed microbes 1. Express perforin to make Holes in Cell membrane 2. Express FasL and **granzyme** **B** to kill cells 3. Express FcR to stimulate AB-dependent cellular cytotoxicity
65
what are Eosinophils 2 main jobs?
They are for parasitic infection and allergic reactions
66
What are Basophils important for? What are they similar to?
They infiltrate sites of allergic Reactions, release mediators and cytokines they are least abundant. They are structurally and functionally similar to mast cells - activated by IgG like mast cells. And recruit cytokines
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