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Immunology > Immuology (Week 2 and 3) > Flashcards

Immuology (Week 2 and 3) Flashcards

1
Q

Cells of the immune system (3 categories)

A

Granulocytes: neutrophils, eosinophils, basophils, mast cells

Myeloid cells: monocyte/macrophage, dendritic cell

Lymphocytes: NK, Th, CTL, B, Plasma cell

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2
Q

4 chemical components of the immune system (4 C’s)

A

Cytokines- Interleukins, interferons, TNF, colony stimulating factor
Compliment-attack extracellular pathogens
Chemokines-leukocyte migration to target site
Coagulation -blood clotting; can modulate immune response

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3
Q

the immune system is a _____organ and ____ _____ unit

A

sensory organ

special forces unit

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4
Q

Physical barrier defense:

A

skin, mucosal epithelia, coughing vomiting

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5
Q

Chemical barriers:

A

pH of body fluids, secreted fatty acids, antimicrobial peptides, ROS

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6
Q

Restricted germline-encoded receptors:

A

TLR (PRRs: pattern recognition receptors). Each TLR recognizes one type of microbial component.

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7
Q

What are PAMPS/DAMPS?

A

Pathogen-associated molecular patters

Damage-associated molecular patterns

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8
Q

Where are PAMPS expressed?

A

cell surface and intracellularily (ex. viruse PAMPS are recognized by intracellular TLRs, same with intracellular bacteria)

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9
Q

PAMP/DAMP + TLR=

A

downstream signaling cascade that results in function of innate cell to deal with the danger (cytokine expression and release, phagocytosis etc. )

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10
Q

What is the inflammasome?

A

multiple cytoplasmic molecules assembled in pinwheel; sensor of danger signals (PAMPS, DAMPS). ex. : results in secretion of IL-1

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11
Q

What are the ‘professional phagocytes’ ?

A

neutrophils, macrophages, dendritic cells, B cells

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12
Q

Name the different types of recognition receptors on the surface of macrophages:

A
  • mannose receptor
  • compliment receptor (binds compliment)
  • Fc receptor (binds antibodies)
  • TLR (PRR)
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13
Q

Phagocytosis leads to…

A

degradation, processing, presentation of antigen (T cell activation), induces pro-inflammatory cytokine release.

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14
Q

Mechs for pathogen elimination:

A
  • phagocytosis
  • compliment cascade
  • ADCC (antibody- dependent cell-mediated cytotoxicity)
  • defensins
  • pentraxins
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15
Q

What does activated compliment do? (3 things)

A
  • recruits inflammatory cells
  • opsonization of pathogens
  • killing pathogens
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16
Q

What does the ADCC- antibody dependent cell-mediated cytotoxicity do? What cells do this?

A
  • Kills opsonized target cells (covered w Abs)

- NK cells, neutrophils, eosiniphils

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17
Q

What are tissue sentinel cells?
What do they express?
Are they recruited first?

A
  • mast cells and epithelial cells
  • PRRs (recognize PAMPS for fast response)
  • Yes, they are first to be recruited.
18
Q

After the tissue sentinel cells, who arrives on the scene?

A

Neutrophils (PMN)

19
Q

Describe neutrophils (PMN).

A
  • large reserve in bone marrow
  • circulate in blood until called on to enter infected tissue
  • dedicated killers (phagocytose)
  • short-lived (die–> Pus.
20
Q

What is the order of innate cells on the scene? TSC, Macrophages, Neutrophils

A

TSC, Neutrophils, Macrophages

21
Q

What doe macrophages do?

A
  • Suppress PMN efflux

- phagocytose pathogens and PMN debris.

22
Q

At sites of inflammation, what pro-inflammatory cytokines do macrophages secrete?

A

IL-1B: activates vascular endothelium, activates lymphocytes, local tissue destruction, increases access of effector cells–> fever, production of IL-6

TNF-a: activates vascular endothelium, increases permeability (inc entry of IgG, compliment, cells to tissue), inc fluid drainage to lymph nodes–> fever, mobilization of metabolites, shock.

IL-6: lymphocyte activation and increased Ab production –> fever, induces acute-phase protein production by hepatocytes

CXCL8: chemotactic factor recruits neutrophils/basophils/T cells to infx site

IL-12: activates NK cells, induces differentiation of CD4 cells into TH1 cells.

23
Q

What organs do IL-1, IL-6, TNF-a act on (what do they do)?

A

Liver: Acute-phase proteins (C-reactive protein, mannose binding protein)–> activation of compliment, opsonization

Bone-marrow endothelium: neutrophil mobilization–> phagocytosis

Hypothalamus: increased body temperature–> decreased viral + bacterial replication, increased antigen processing, facilitates adaptive immune response

Fat, muscle: protein and energy mobilization to generate increased body temperature–> ‘’

Dendritic cells: TNF-a stimulates migration to lymph nodes and maturation–> initiation of adaptive immune response

24
Q

What do Natural Killer Cells do?

A
  • killer lymphocytes of innate immune response
  • provide innate immunity against intracellular infx, esp virus
  • cytokine production
  • killing fnx (ADCC)
25
Q

What do dendritic cells do?

A
  • immature DC phagocytose
  • activated via TLR
  • DC mature and release pro-inflammatory cytokines.
  • important link bw innate and adaptive immunity (APC–> activates naive T cells)
26
Q

Name and describe the 3 compliment pathways:

A

Classical pathway: Ag:Ab complexes–> compliment activation–> recruits inflamm cells, opsonization, killing pathogens

MB-Lectin pathway: lectin binds pathogen surface–> ‘’

Alternative pathway–> pathogen surfaces–>’’

27
Q

Describe the mediators involves in all 3 compliment pathways and the convergence compound.

A

Classical: C1q, C1r, C1s, C4, C2

MB-Lectin: MBL, MASP-1, MASP-2, C4, C2

Alternative: C3, B, D

Convergence: C3 convertase (C3–> C3a + C3b)

28
Q

C3–> C3a + C3b, what does each do?

A

C3a: small soluble fragment, causes inc vascular permeability and recruitment/activation of phagocytes= anaphylitoxin (drives inflammation)

C3b: covalently tags bacteria, enhances recognition/phagocytosis/killing of pathogen by PMN+macrophages= opsonisation

29
Q

What are the two anaphylatoxins mentioned? What do they do?

A

C3a and C5a

increase vascular permeability and activate phagocytic cells–> extravasation of compliment and other proteins at infx site, migration of monocytes and neutrophils from bld to tissue inc. Incs microbicidal activity of macrophages and neutrophils.

30
Q

What does C1, compliment compound, do?

A

binds to Ab-Ag complexes

31
Q

What is the activation cascade for creating C3 convertase?

A

C1 binds Ag:Ab–> C1 active

C1 + C4–> C4a + C4b

C4b + C2–> C3 convertase

32
Q

What do C3a, C3b and C5b/C6/C7/C8/C9 do?

A

C3a: peptide mediators of inflammation, phagocyte recruitment (anaphylotoxin)

C3b: binds compliment receptors on phagocytes–> opsonization of pathogens, removal of immune complexes

C5b-C9: MAC, lysis of pathogens and cells

33
Q

How does C3 convertase contribute to the MAC activity?

A

C3 convertase–> C5 convertase + C5 –> C5a + C5b

C5b+ C6/7/8/9–> MAC

34
Q

What autoimmune disease is C4 deficiency associated with?

A

Systemic Lupus Erythmatosus

35
Q

True or false: deficiency in C4 and other early components (C1, C2) do not predispose to severe infx.

A

True.

36
Q

What bacterial infx are individuals with deficient late compliment components (C5-9) susceptible to?

A

Infx with genus Neisseria

i.e. Gorrnorrhea, Meningitis.

37
Q

What does a deficiency in C3 and other factors that opsonize result in (clinically)?

A

recurrent pyogenic infx

high rate of morbidity and mortality

38
Q

What deficiency causes: Hereditary Angioneurotic edema?

A

C1INH deficiency (C1INH inactivates C1 complex)–. love C1INH leads to higher C1 activity–. more C2, C4. When stressed px has excessive C1 building…inc in C2 fragments–> vasoactive peptides–> swelling

39
Q

What do you know about febrile neutropenia?

A

-due to chemotherapy often
-failed innate innumity
-high risk of infx (esp w <500 cells/microL)
lack of pus and classical signs of inflammation mean infx less obvious
-can be life threatening; treat empirically with antibiotics

40
Q

what characterizes autoinflammatory syndromes?

A
  • arise from single gene mutations
  • inappropriate activation of innate inflammatory mechs
  • recurrent fevers, rash, serositis, arthritis, no evidence of infx

Immunology (32 decks)

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