Immuno 5: Innate Immunity

Front 1

5 groups of antigens that can cause disease:

Back 1

1) viruses

2) bacteria

3) fungi

4) protozoa

5) worms

*worms and protozoa are usually grouped together and called parasites.

Front 2

Over what time period do innate immune responses function?

Back 2

Althoughthese responses are most important over the first 4 days (96 hrs), beaware that these responses will continue until the pathogen is cleared.

Front 3

Name the mechanical barriers that are part of the initial innate immune response.

Back 3

Skin - Flow of fluid, perspiration, and sloughing off of skin.

GI - Flow of fluid, mucus, food, and saliva

Respiratory tract - Flow of fluid and mucus by cilia, air flow

GU - Flow of fluid, urine, mucus, and semen

Eyes - Flow of fluid, tears.

*Epithelial cells joined by tight junctions in all categories listed above.

Front 4

Name the chemical barriers that are part of the initial innate immune response.

Back 4

Skin - sebum (fatty acids, lactic acid, lysozyme)

GI - Acidity, enzymes (proteases)

Respiratory tract - Lysozyme in nasal secretions

GU - acidity in vaginal secretions; Spermine and zinc in semen

Eyes - Lysozyme in tears.

*Antimicrobial peptides (defensins) from all categories listed above.

Front 5

Name the microbiological barriers that are part of the initial innate immune response.

Back 5

Normal flora of skin, GI tract, Resp tract, GU tract, and eyes.

Front 6

Name the term for amphipathic molecules that form pores in the surface of the pathogens resulting in osmotic disintegrity and death of the microbe?

Back 6

defensins

*Know that there are many different types.

Front 7

What is one of the primary source of defensins in the gut?

Back 7

Paneth cells

Front 8

Initital innate immune response time period (ubiquitous response):

Back 8

0-4 hrs after exposure.

Front 9

Induced responses of innate immunity (bacterial vs. viral control) time period:

Back 9

4 hrs-96 hrs post exposure.

Front 10

What does the cytokine monster, IL-1, IL-6, TNF-alpha do?

Back 10

-initates the acute phase response.

-initiates neutrophil mobilization by acting on bone marrow endothelium. Results in increased phagocytosis.

-increases body temperature (fever) by acting on hypothalamus, fat, and muscle.

Front 11

Products of the acute-phase repsonse:

Back 11

C-reactive protein (CRP) and Mannose-binding protein (MBP) are upregulated in the liver.

-induction of fever is also an important feature.

Front 12

Which phagocyte is recruited in the most abundance to an infected site?

Back 12

neutrophils

Front 13

What surface adhesion molecules are on neutrophils and on surface of the vascular endothelium that help neutrophils go through the endothelial layer?

Back 13

Adressins on neutrophils bind to selectins on surface of the vascular endothelium.

Front 14

Name the 2 steps of the respiratory burst

Back 14

1st step - fusion of phagosome with azurophilic granules that contain antimicrobials. (myeloperoxidase, lysozyme, elastase, antimicrobial peptides)

2nd setp - fusion of phagosome with lysosomes (degradative enzymes such as acid hydrolases)

Front 15

What do phagocytes and some bacteria make to interfere with the damaging effects of the respiratory burst?

Back 15

Catalase - limits damaging effects of toxic oxygen species.

Front 16

What does NADPH oxidase do?

Back 16

It produces superoxide radicals that are later converted to H2O2.

*NADPH oxidase is created once lysosome granules fuse with the phagosome.

Front 17

NETosis

Back 17

A type of cell death neutrophils can undergo that results in expulsion of chromatin and digestive enzymes to form an extracellular net.

It prevents dissemination and can kill bacteria.

Front 18

Pattern Recognition Receptors (PRRs)

Back 18

Host cell receptors that bind to common features of pathogens; known as PAMPs.

Front 19

What happens macrophages recognize PAMPs via their PRRs?

Back 19

-triggered to phagocytose material

-produce inflammatory cytokines

-begin to express B7 (co-stimulator) on their surface

Front 20

Describe endocytic PRRs

Back 20

They promote phagocytosis of microorganisms by phagocytes without relaying an intracellular signal.

-primarily recognize carbohydrates

Ex. of endocytic PRRs: mannose receptors, glucan receptors, scavenger receptors

Front 21

Define the 3 types of signaling PRRs:

Back 21

-Toll-like (TLRs) - membrane bound proteins, recognize microbial constituents, initiate cytokine production.

-NOD-like (NLRs) - cytoplasmic proteins, recognize microbial products, initiatie cytokine production.

-RIG-1 like (RLRs) - cytoplasmic proteins, sense viral RNA

Front 22

TLR2/TLR6 bind to:

Back 22

-lipoteichoic acid (gram-positive bacteria)

-zymosan (fungi)

Front 23

TLR3 binds to:

Back 23

double stranded viral RNA

Front 24

TLR4/TLR4 (TLR4 homodimers) bind to:

Back 24

LPS (gram negative bacteria)

Front 25

TLR-7 and TLR-8 bind to:

Back 25

single-stranded viral RNAs

Front 26

Describe secreted PRRs:

Back 26

Secreted from host cells.Examples: C-reactive protein and mannose binding protein/lectin.

Front 27

What does CRP do after beng released form the liver?

Back 27

Binds to phosphocholine residues unique to bacterial surfaces, and when bound it becomes a ligand for binding by complement component C1. This initiates the classical complement cascade.

Front 28

Role of TNF alpha:

Back 28

-activates vascular endothelium causing leakage of fluids into tissues.

-increased plateled adhesion to the walls of the small blood vessels.

-occlusion of the blood vessel and prevention of bacteria from disseminating via the blood.

-This buys time form local phagocytes to engulf and kill the organisms.

Front 29

Why can TNF alpha cause septic shock?

Back 29

It acts systemically so small vessels all over the body become occluded due to a combination of reduced blood volume and increased platelet adhesion. Many of them collapse.

Front 30

What do interferons released by virus-infected host cells do to help?

Back 30

-make adjacent cells less susceptible to infection.

-induce increased expression of MHC Class I and other ligands for the inhibitory receptors on NK cells on surrounding cells. (so NK cells won't are less likely to kill them)

-activate NK cells

Front 31

IFN-alpha, IFN-beta are:

Back 31

interferons released by virus-infected host cells.

Front 32

What do NK cells receptors recognize on virus-infected cells that causes them to degranulate?

Back 32

-inhibitory receptors recognize: a decrease in MHC Class I proteins that happens late.

-activating receptors recognize: MIC proteins that are expressed by stressed cells (MIC-1 and/or MIC-2) early on