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IHL test 1 > Innate Immunity > Flashcards

Flashcards in Innate Immunity Deck (16):

Which type of immunity has Toll-like receptors, mannose receptors and NOD-like receptors? How do the cells get these receptors?

Innate, they are coded in germline of cell.


Which type of immunity has TCR receptors? How do they get them?

Adaptive. produced by somatic recombination of gene segments. More diversity than innate.


What are Defensins and cathelicidins and where does it fit into immunity?

what produces them?

antimicrobials. Part of the chemical barrier in innate immunity. Kills bacteria, virus, fungi with local abx

Neutrophils and Paneth cells


Where do you find Pattern Recognition Receptors (PRR)?

Innate immunity. Extracellular, Cytosolic and endosomal.

Born with these, recognized about 1,000 patterns
ex. Pilin, flagellin, LPS, ssRNA, CpG, Lipoteichoic acid, glucans, mannan


Which TLR are on extracellular of leukocytes? which are endosomal?

Extracell- TLR 1, 2, 4, 5, 6
Endosomal- TLR 3, 7, 8, 9

NOD like- similar but cytosolic.


What happens when a TLR finds a pathogen?

Increase microbicidal activity and apoptosis.

Produce defensins


What is the goal of the TLR signaling pathway?

What two transcription factors does it activate?

Promote inflammation and/or antiviral state.

1. NF-kB > increase cytokines, adhesion molecules, costimulators > acute inflammation, stimulate adaptive immunity.

2. IRFs (Interferon regulatory factors) > produce IFN a, B (Type I) > Antiviral state, send signal to other cells to creat barrier so not infected.


What is DAMP?

Damage-associated Molecular Patterns, (danger signal)

released by necrotic cells. Promote inflammatory response

Increase in serum levels of DAMPs associated with many inflammatory diseases: sepsis, arthritis, atherosclerosis, lupus, Chron's, Cancer.


Macrophages release these, what do they do?

IL-1B and TNF-alpha

IL-1B/TNFalpha: induce blood vessels to be more permeable, allowing effector cells to enter infected tissue.

IL-6 Induce fat/muscle cell to metabolize, make heat and raise the temp in the infected tissue

CXCL8: Recruit neutrophil from blood, guide to tissue

IL12: Recruits and activates NK cells which secrete cytokines to increase response of macrophage to infection


What is Chronic Granulomatous disease?

Usually Neutrophils kill microbes with pH, enzymes and ROS

In chronic granulomatous disease neutrophils can't kill what they ate (genetic defect)


What do mast cells secrete? and what does it do?

Mast cells secrete histamine (vasodialator), amplifies inflammation


What do Natural Killer cells secrete? What does it do?

IFN-y: activates macrophages.

(IL 12 is released from macrophages and recruites/activates NK cells)


TNF-alpha, Normal and systemic

Usually cause inflammation (increase permeability.. )

Systemic infection (sepsis): macrophage release TNFalpha into blood stream > systemic edema > too much plasma out of blood > decrease blood volume, hypoproteinemia and neutropenia > collapse of vessels > Disseminated Intravascular coagulation leads to waisting and multiple organ failure: septic shock.


What do IFN-a and IFN-B (cytokines) do?

Triggered by virus infected cell.
Induce resistance to viral replication in all cells.
Increase expression for ligand for receptors on NK cells.
Activate NK cells to kill virus-infected cells.


Leukocyte Adhesion Deficiency I

What is going on and what are the symptoms?

IL-1 and TNF increase expression of P & E selections on endothelium, bind and slowing down (rolls) leukocytes so cytokines can hit it stimulate migration.

In LAD I integrin on leukocyte is deficient, can't attach to endothelial receptors, no migration to infected site

Delayed separation of umbilical cord.
recurrent bacterial infections, in skin and mucosa
Periodontitis (later)
Impaired wound healing
Absent pus formation.


What is contraction? What players are involved (4)?

When pathogen is cleared, need to heal and decrease inflammation

IL-1 receptor antagonist
Suppressor of cytokine signaling (SOCS) proteins
Alternative C' pathway inhibitors