Immune System 2 Flashcards
What are Interferons?
Interferons are proteins produced by cells infected with viruses to “interfere” with viral replication
What is a Type 1 Interferon?
3
- When a cell becomes infected by a virus, it can produce and release Type I interferons into the extracellular fluid
- These released interferons can then bind to the surface of neighboring, non-infected cells
- This triggers the non-infected cells to produce antiviral proteins that can prevent viral replication if cell becomes infected (Can work in most cells as long as they have type I interferon receptor)
What is a Type II interferon or Interferon-Gamma?
- Type II Interferon can Potentiate (increase efectiveness) of Type I Interferon
- It releases Cytokines to increase Proliferation
- Proliferation increases the numbers of some immune cells and the secretion of cytotoxic chemicals, which can kill pathogens (Involved in “activated” versions of macrophages and NK cells)
What are Cytokines?
small proteins that act in cell signalling/communication
What is Phagocytosis?
Phagocytosis is a vital cellular process in which certain cells engulf and digest solid particles, such as pathogens, cellular debris, or other foreign materials
What is a Phagocyte?
Phagocyte – any cell that can do phagocytosis
What are Neutrophils?
quick response
Quick Response:
Neutrophils are a type of white blood cell (granulocyte) and are known for their rapid response to infections. They are among the first cells to arrive at the site of infection or inflammation.
Short Lifespan:
Neutrophils have a relatively short lifespan but are highly effective at engulfing and destroying pathogens. They release antimicrobial substances and enzymes to break down ingested material.
What are Macrophages?
largest capacity
Largest Capacity:
Macrophages are also white blood cells (monocytes) that have matured and become tissue-resident. They are versatile phagocytes found in various tissues throughout the body.
Phagocytic Efficiency:
Macrophages have a larger phagocytic capacity compared to neutrophils. They are efficient at phagocytosing a wide range of particles, including pathogens and cellular debris
What are the 4 Phases of Phagocytosis?
- Recognition
- Ingestion
- Digestion
- Kill
4 Phases of Phagocytosis
What is Recognition?
Recognition – The pathogen binds on to the cell membrane of phagocyte
4 Phases of Phagocytosis
What is Ingestion?
3
Ingestion - The phagocyte engulfs the recognized pathogen by extending its cell membrane around the particle.
This engulfment process can be described as phagocytosis or endocytosis
Outcome:
The engulfed pathogen is now enclosed in a vesicle called a phagosome, which is an internal compartment within the phagocyte
4 Phases of Phagocytosis
What is Digestion?
3
The phagosome formed during ingestion undergoes maturation by fusing with lysosomes creating a phagolysosome
The contents of the lysosome, including digestive enzymes, now come into contact with the engulfed pathogen.
Digestion of the pathogen occurs within the phagolysosome, breaking it down into smaller, more manageable components.
What is a phagolysosome?
phagosome infused with lysosome
4 Phases of Phagocytosis
What is the Kill Phase?
2
The final phase involves the destruction of the pathogen.
The pathogen is rendered non-functional, and the end products of digestion are either released internally within the phagocyte for further processing or expelled from the cell through exocytosis.
What are Complement Proteins?
Complement proteins are Plasma Proteins produced in the liver and continually circulating inactive in blood
Activated proteins “complement” or enhance immune reactions
30 compliment proteins
What is the Function of Compliment Protein 3 (C3)?
In response to encountering a pathogen, inactive C3 binds to the pathogen’s surface. This binding activates C3, initiating a cascade of events that involve the sequential activation of various complement proteins.
This cascade amplifies the immune response, leading to the opsonization of the pathogen and the initiation of a series of reactions that contribute to the pathogen’s elimination.
What is Opsonization?
Opsonization refers to the process by which particles, such as pathogens, are coated with molecules that enhance their recognition and engulfment by immune cells
How does C3 function in Osponization?
Opsonization by attachment of portion of C3 (C3b) to pathogen:
- Enhances phagocytosis.
- Opsonin (marker) – makes easier to recognize
What other Complement Proteins Does C3 activate? What does this create?
C3 actiavtes C5, C6, C7, C8 & C9.
The activated version of these Complement Proteins make up the Membrane Attack Complex (MAC) that inserts on to the cell membrane of the targeted pathogen
What does the Membrane Attack Complex (MAC) do once on membrane?
The MAC creates pores or channels in the membrane of the pathogen.
The pores formed by the MAC allow the unregulated influx of fluids and other molecules into the pathogen’s intracellular environment.
This Kills the Pathogen
What is Inflammation or inflammatory response?
local responses to tissue damage
What are Sources of Inflamation?
(5)
- Pathogens (such as bacteria, viruses, or fungi).
- Abrasions or physical injuries.
- Chemical irritants.
- Cell distortion or disturbance.
- Extreme temperatures (heat or cold)
Response is remarkably similar no matter the source
What are some Charcteristic Symptoms of Infalmmation?
redness, pain, heat, swelling (also loss of tissue function in damage area sometimes
What Responds to Inflammation?
What is their Goal?
Often resident immune cells (like fixed macrophages) at injury location but may not be enough – cells will need to migrate to site
Goals - isolate, destroy or inactivate invader / remove debris / prepare for wound healing and tissue repair.
What occurs in the 1st Stage of Inflammation? What is Released?
Release of inflammatory mediators:
Histamine, Kinins, Prostaglandins, Complement Proteins Cytokines, etc.
1st Stage of Inflammation
What Local effects are Triggered?
2
Trigger – local effects
- Vasodilation microcirculation:
increases blood flow for delivery of leukocytes, plasma proteins, nutrients, oxygen, etc. (outward signs: local redness, heat). - Increased permeability of blood vessels: endothelial cells contract opening spaces between them
1st Stage of Inflammation
What Non-Local effects are Triggered?
(2)
Trigger – non-local effects
- Release of stored immune cells (spleen, lymph nodes) into circulation.
- Proliferation (increasing numbers) of new immune cells in bone marrow.
What occurs in the 2nd Stage of Inflammation?
- Phagocyte movement into injury site from blood (starts within 1 hour).
- Neutrophils early, later circulating monocytes mature into wandering macrophages
2nd Stage of Inflammation
What are the 3 Steps?
- Margination
- Diapedesis
- Chemotaxis
2nd Stage of Inflammation
What occurs in Margination and Diapedesis?
Margination:
- phagocytes and local endothelium each form adhesion molecules for attachment to local area.
Diapedesis:
- phagocyte migration through blood vessel walls into interstitial fluid
2nd Stage of Inflammation
What occurs during Chemotaxis?
Chemotaxis:
phagocyte migration to injury site guided by cytokines (chemoattraction).
- Fluid follows; local distension (outward signs: some edema/swelling, pain).
- Cytokines can come from a number of sources and attract many needed things / timing of release important to timing of attraction
What is the 3rd Stage of Inflammation?
- Worn out, damaged, or dead cells replaced.
- May include new network of small blood vessels (angiogenesis) to help remove debris and deliver needed nutrients and oxygen
3rd Stage of Inflammation
What happens after Tissue Repair?
- Tissue repair may leave no sign or in other cases a scar (scar tissue often less functional: denser collagen fibers, decreased elasticity, fewer blood vessels).
- Remodelling may continue after initial repair.
