Immuology (Week 2 and 3) Flashcards Preview

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Flashcards in Immuology (Week 2 and 3) Deck (40):
1

Cells of the immune system (3 categories)

Granulocytes: neutrophils, eosinophils, basophils, mast cells

Myeloid cells: monocyte/macrophage, dendritic cell

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

2

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

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

3

the immune system is a _____organ and ____ _____ unit

sensory organ
special forces unit

4

Physical barrier defense:

skin, mucosal epithelia, coughing vomiting

5

Chemical barriers:

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

6

Restricted germline-encoded receptors:

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

7

What are PAMPS/DAMPS?

Pathogen-associated molecular patters

Damage-associated molecular patterns

8

Where are PAMPS expressed?

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

9

PAMP/DAMP + TLR=

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

10

What is the inflammasome?

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

11

What are the 'professional phagocytes' ?

neutrophils, macrophages, dendritic cells, B cells

12

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

-mannose receptor
-compliment receptor (binds compliment)
-Fc receptor (binds antibodies)
-TLR (PRR)

13

Phagocytosis leads to...

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

14

Mechs for pathogen elimination:

-phagocytosis
-compliment cascade
-ADCC (antibody- dependent cell-mediated cytotoxicity)
-defensins
-pentraxins

15

What does activated compliment do? (3 things)

-recruits inflammatory cells
-opsonization of pathogens
-killing pathogens

16

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

-Kills opsonized target cells (covered w Abs)
-NK cells, neutrophils, eosiniphils

17

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

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

18

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

Neutrophils (PMN)

19

Describe neutrophils (PMN).

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

20

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

TSC, Neutrophils, Macrophages

21

What doe macrophages do?

-Suppress PMN efflux
-phagocytose pathogens and PMN debris.

22

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

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

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

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

What do Natural Killer Cells do?

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

25

What do dendritic cells do?

-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

Name and describe the 3 compliment pathways:

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

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

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

C3--> C3a + C3b, what does each do?

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

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

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

What does C1, compliment compound, do?

binds to Ab-Ag complexes

31

What is the activation cascade for creating C3 convertase?

C1 binds Ag:Ab--> C1 active

C1 + C4--> C4a + C4b

C4b + C2--> C3 convertase

32

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

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

How does C3 convertase contribute to the MAC activity?

C3 convertase--> C5 convertase + C5 --> C5a + C5b

C5b+ C6/7/8/9--> MAC

34

What autoimmune disease is C4 deficiency associated with?

Systemic Lupus Erythmatosus

35

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

True.

36

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

Infx with genus Neisseria

i.e. Gorrnorrhea, Meningitis.

37

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

recurrent pyogenic infx

high rate of morbidity and mortality

38

What deficiency causes: Hereditary Angioneurotic edema?

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

What do you know about febrile neutropenia?

-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

what characterizes autoinflammatory syndromes?

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