Chapter 3 Vocab

Question 1

Self

Answer 1

The cells of our body that we can differentiate from pathogens or infected cells due to various differences such as membrane composition

Question 2

Non-self

Answer 2

Pathogens or infected cells recognizable by differences in their cell membranes, proteins they express, or in the structure of their nucleic acids

Question 3

Mannose Receptor

Answer 3

a type of receptor on the surface of macrophages that help mediate endocytosis of pathogens before returning to the surface

Question 4

Scavenger Receptors

Answer 4

A large family of receptors of the surface of pathogens that can recognize the broad details of pathogens (ex. bacteria vs. fungi vs. virus)

Question 5

Toll-like receptors (TLRs)

Answer 5

A type of signaling receptor that recruits other immune cells upon binding to PAMPs. TLRs are often dimers with domains that have a high leucine content. They can work in concert with other receptors to identify PAMPs. They signal by recognizing the pathogen, changing their conformation, initiating a signaling cascade, and then initiating transcription of proper responses.

Question 6

MyD88

Answer 6

an adapter protein that can bind other proteins and activate them

Question 7

Kinase cascade

Answer 7

a signaling cascade that involves phosphorylation of proteins

Question 8

NFkb

Answer 8

a transcription factor that activates transcription of genes for inflammatory cytokines

Question 9

PAMPs

Answer 9

pathogen associated molecular patterns; recognizable by receptors on our cells

Question 10

Pro-inflammatory cytokines

Answer 10

a type of cytokine produced by macrophages that induce inflammation; aka chemokines

ex. IL-1 beta

Question 11

CXCL8

Answer 11

a chemokine that recruits neutrophils and directs them to sites of infection

Question 12

IL-12

Answer 12

an inflammatory cytokine (chemokine) that induces NK cells to migrate to sites of infection

Question 13

IL-1

Answer 13

a key inflammatory cytokine that helps induce formation of the inflammasome

Question 14

TNF-alpha

Answer 14

an inflammatory cytokine that promotes vascular permeability, which is important for the local recruitment of effector cells and the influx of serum proteins

overproduction throughout the body can lead to septic shock

It also attracts NK cells and induces fever (is a pyrogen)

Question 15

IL-1 beta

Answer 15

a pro-inflammatory cytokine

Question 16

Chemokines

Answer 16

pro-inflammatory cytokines

Question 17

Pyroptosis

Answer 17

Pyroptosis is a form of cell death that sees inflammasomes active gasdermin D pores. Upon pyroptosis, the macrophages release large amounts of IL-1b.

Question 18

Septicemia

Answer 18

a systemic infection of the bloodstream

Question 19

Septic shock

Answer 19

The result of a systemic infection that sees TNF-alpha produced throughout the body, leading the collapse of the cardiovascular system.

Systemic edema caused by TNF-alphas causes decreased blood volume, hypoproteinemia, neutropenia, and neutrophilia. Decreased blood volume causes collapse of vessels. Disseminated intravascular coagulation leads to wasting and multiple organ failure.

Question 20

Lectins

Answer 20

a type of adhesion molecule (cell surface proteins) that recognizes carbohydrate structure

Question 21

Integrins

Answer 21

a type of adhesion molecule that recognizes protein partners

Question 22

Vascular addressins

Answer 22

a type of adhesion molecule that help neutrophils roll along the endothelium

Question 23

Diapedesis

Answer 23

the passage of blood cells through the intact walls of the capillaries, typically accompanying inflammation.

Question 24

Extravasation

Answer 24

the process by which neutrophils migrate from the blood stream into infected tissues

Question 25

Respiratory burst

Answer 25

the production of reactive oxygen species

Question 26

Chronic Granulomatous Disease

Answer 26

a disease resulting from a defect in respiratory burst; prevents neutrophils from killing pathogens, so the immune system walls them off in granulomas

Question 27

Netosis

Answer 27

mechanism by which the death of neutrophils produces neutrophil extracellular traps (NETs) that trap and kill pathogens. The neutrophil nucleus swells and bursts, the chromatin dissolves and becomes extruded from the cell in a network of decondensed DNA.

Question 28

Fever

Answer 28

Rise of body temperature above the normal range caused by cytokines called pyrogens produced in response to infection. Fevers are good because they slow the growth of pathogens since most of them are adapted to growth at lower temperatures. Additionally, innate immune responses are enhanced at higher temperatures.

Question 29

Pyrogens

Answer 29

any molecule that induce fever, such as some cytokines or bacterial products

Question 30

Acute phase proteins

Answer 30

Acute phase proteins are proteins produced in response to the inflammatory mediator IL-6. They help opsonize pathogens and activate complement.

Examples are CRP and MBL

Question 31

C Reactive protein

Answer 31

C-reactive protein is a pentamer made up of five indentical subunits. It binds phosphocholine in the membranes of pathogens. C-reactive protein is involved in the classical pathway

Question 32

Mannose binding lectin

Answer 32

Mannose-binding-lectin contains mannose binding sites that interact with mannose on the surface of pathogens. It is involved in the lectin pathway of complement activation

Question 33

MASP1 and MASP2

Answer 33

proteases involved in the lectin pathway; MASP2 cleaves C4 to C4a and C4b and also cleaves C2 to C2a and C2b

Question 34

C1 complex

Answer 34

a complex that is involved in the classical pathway; it binds to C reactive protein; has protease activity, cleaves C4 and C2

Question 35

Classical C3 convertase

Answer 35

The enzyme complex C2aC4b that can cleave C3 into C3a and C3b. It is not as efficient as the alternative C3 convertase, so that is why it makes it during the classical and lectin pathways of complement activation