Chapter 3 Vocab Flashcards
Self
The cells of our body that we can differentiate from pathogens or infected cells due to various differences such as membrane composition
Non-self
Pathogens or infected cells recognizable by differences in their cell membranes, proteins they express, or in the structure of their nucleic acids
Mannose Receptor
a type of receptor on the surface of macrophages that help mediate endocytosis of pathogens before returning to the surface
Scavenger Receptors
A large family of receptors of the surface of pathogens that can recognize the broad details of pathogens (ex. bacteria vs. fungi vs. virus)
Toll-like receptors (TLRs)
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.
MyD88
an adapter protein that can bind other proteins and activate them
Kinase cascade
a signaling cascade that involves phosphorylation of proteins
NFkb
a transcription factor that activates transcription of genes for inflammatory cytokines
PAMPs
pathogen associated molecular patterns; recognizable by receptors on our cells
Pro-inflammatory cytokines
a type of cytokine produced by macrophages that induce inflammation; aka chemokines
ex. IL-1 beta
CXCL8
a chemokine that recruits neutrophils and directs them to sites of infection
IL-12
an inflammatory cytokine (chemokine) that induces NK cells to migrate to sites of infection
IL-1
a key inflammatory cytokine that helps induce formation of the inflammasome
TNF-alpha
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)
IL-1 beta
a pro-inflammatory cytokine
Chemokines
pro-inflammatory cytokines
Pyroptosis
Pyroptosis is a form of cell death that sees inflammasomes active gasdermin D pores. Upon pyroptosis, the macrophages release large amounts of IL-1b.
Septicemia
a systemic infection of the bloodstream
Septic shock
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.
Lectins
a type of adhesion molecule (cell surface proteins) that recognizes carbohydrate structure
Integrins
a type of adhesion molecule that recognizes protein partners
Vascular addressins
a type of adhesion molecule that help neutrophils roll along the endothelium
Diapedesis
the passage of blood cells through the intact walls of the capillaries, typically accompanying inflammation.
Extravasation
the process by which neutrophils migrate from the blood stream into infected tissues
Respiratory burst
the production of reactive oxygen species
Chronic Granulomatous Disease
a disease resulting from a defect in respiratory burst; prevents neutrophils from killing pathogens, so the immune system walls them off in granulomas
Netosis
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.
Fever
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.
Pyrogens
any molecule that induce fever, such as some cytokines or bacterial products
Acute phase proteins
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
C Reactive protein
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
Mannose binding lectin
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
MASP1 and MASP2
proteases involved in the lectin pathway; MASP2 cleaves C4 to C4a and C4b and also cleaves C2 to C2a and C2b
C1 complex
a complex that is involved in the classical pathway; it binds to C reactive protein; has protease activity, cleaves C4 and C2
Classical C3 convertase
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
