Unit 1 Flashcards
Pathogens enters on what side to what side?
Afferent lymphatic vessel to the efferent lymphatic vessel
Why do lymph nodes swell?
B cells and T cells are replicating their other lymph cells
Steps of when someone gets a cut
1- Macrophages come and eat large pathogens
2-Dendrites eat smaller pathogens
3- They travel down the lymph ducts
4- into the lymph nodes and look for matching T cells and B cells.
If not found,
5- They keep moving along the line until they find the right lymph node
What does the spleen filter?
Blood. Removes blood Bourne pathogens, damaged or dead red blood cells
Cells that stimulate B and T cells arriving in the spleen
Splenic macrophages and dentritic cells
Asplenia
People born without spleens. They are very susceptible to infections
Pulp where RBC are monitored and removed
Red pulp
Pulp in spleen where WBC gather
White pulp
Most extensive mucosal surface of the body
Gut
Gut associated lymphoid tissues (GALT)
Tonsils, adenoids, appendix, peyer’s patches
Function of the GALTS, BALTs, and MALTs
Filter out pathogens to activate lymphocytes. M cells deliver pathogens across the mucosa for delivery to lymphocytes to be activated.
Physical and chemical barriers
Skin
Mucosal epithelium
Baby’s have no _____ in utero until birth
Flora, or anything in the gut
Commensalism microorganisms function
Colonize the skin and mucosa
Optimal commensalism action because of the reliable food source
Gut
2 categories of infection
Intracellular infections and extracellular infections
Most bacteria is this type of infection, as well as fungi and parasites
Extracellular
Infection subject to soluble secreted molecules of the immune system
Extracellular infection
Infection inside the cell. Once the cell is infected, the whole cell has to die. Typical viral infections
Intracellular infections.
First defense mechanism
A soluble protein
Complement
Where are complements present and where are they made?
Made in the liver
Present in lymphatics and blood
Actions of complements
They coat the surface of bacteria/virus to make them easier or tastier to phagocytise
Some complement proteins are proteases
Key to complement cascade
C3
Upping activation, what happens to C3?
C3 is cleaved into C3a (the smaller molecule) and C3b (The larger molecule)
Inactive form of complements
Zymogens
What C3 binds to the pathogen surface? What is this called?
C3b
Compliment fixation
Which C3 calls for help, and who do they call?
C3a, calls macrophages
Why does C3b bind to pathogens?
It has a high-energy thioester bond in the glycoprotein. This is targeted by water to allow tight fixation to any pathogen surface
3 pathways of complement activation
1- Alternative pathway
2- Lectin pathway
3- Classical pathway (discovered first, but last pathway)
Pathway that works at the start of infection
Alternative pathway
Pathway induced by infection but takes time
Lectin
Pathway that required binding of an antibody or specialized protein (C-reactiv protein) to pathogen surface?
Classical pathway
First step of alternative complement pathway
Hydrolysis of C3 by water or pathogen surfaces
Makes iC3 or C3(H2O)
In alternative complement pathway, C3b molecules:
attach to molecules on the pathogen’s surface
What does C3 convertase do?
Cleaves C3 to make C3a and C3b
Process of C3 converts to C3bBb
C3b binds
B sits on top of C3b. Now C3bB
D comes and sits on tip then breaks B into B.B. and Ba
Bb stays so now is C3bBb
This now goes to cleave other C3s
This is a self-perpetuating process
C3bBb is also knows as:
Alternative C3 convertase
Complement control proteins regulate:
Plasma proteins that interact with C3b on human and microbial cell surfaces which include:
Properdin (factor p)
Factor H
Factor I
Membrane proteins on humans cells that prevent complement fixation on human cells
Properdin action:
Comes along and binds to C3 convertase and improves the entire response. Increases power, speed and efficiency
Factor H
Acts opposite of Properdin. Binds to C3b and promotes cleavage of it by factor I so that is becomes iC3b
Factor I action
Works with Factor H. Decreases C3 convertase molecules on the pathogen surface
What happens when there is no factor I?
C3bBb is unchecked, so all complements are burned through quickly. Causes increases amount of illnesses
Membrane proteins that interfere with complement activation at human cell surfaces
Decay-accelerating factor (DAF)
Membrane cofactors protein (MCP)
DAF action
Binds to C3b and renders it inactive
MCP action
Makes C3b more susceptible to cleavage and inactivation by factor I
Monocytes mature into:
Macrophages
Cell that serves as a part of innate and adaptive immunity
Macrophages
Location of macrophages
On mucosal surfaces and in the lives (Kupffer cells)