Innate Immunity and Inflammation Flashcards
immunity that is the rapid response, non-specific, born with it, works the same way each inflection
involves inflammation
innate immunity
immunity that is complex, has specificity and the ability to remember
mediated by lymphocytes with diverse antigen receptors
either (1) mediated by antibodies from B cells or (2) T cells
adaptive immunity
what is inflammation?
delivery of cells/proteins & fluid into infected tissue, defense against microbes, repair of injured tissue
what is the function of red blood cells and where do they come from?
gas delivery or oxygen and co2
come from bone marrow - hematopoetic stem cell
A type of blood cell that is made in the bone marrow and found in the blood and lymph tissue. Leukocytes are part of the body’s immune system. They help the body fight infection and other diseases. what are the Types?
types of leukocytes are granulocytes (neutrophils, eosinophils, and basophils), monocytes, and lymphocytes (T cells and B cells and NK cells).
cells that are present in the tissue before infection
tissue sentinnel cells
• dendritic cells - bind microbe then secrete variety of proteins, cytokines (pro-inflammatory)
• macrophages in tissues - secrete cytokines too after phagocytosis
• mast cell - bind microbe, has granules in cytoplasm w inflammatory mediators, granules (histamine) & cytokines are released
• all have innate receptors
** secrete pro-inflammatory cytokines
two cells that live in vessles and only go to tissue if it becomes infected
Neutrophils • innate immune receptors on surface • microbes bind to receptor and neutrophil gets activated • phagocytosis (eats microbe) • apoptosis (dies after eating microbe)
Monocytes • macrophage (eat) in the tissue, internalizes microbes • also has the innate receptors • phagocytosis & apoptosis • eats dead neutrophils
role of both = phagocytosis
what is the response of sentinel cells in inflammation?
Epithelial barrier- separating dirty microbe world from tissue within
• sentinel cells in the tissue have innate receptors that recognize the microbes
• sentinel cells get activated, release pro-inflammatory mediators
**So the mediators (cytokines) diffuse and bind to the receptors that line endothelial cells on Blood vessels that run thru the tissues
• receptors are on the endothelial cells
• mediators bind, activation, leukocytes leave blood vessel to go into tissue
• recruitment of circulating leukocytes (monocytes & neutrophils) from blood into tissue
what is the response of blood cells (2 that live in vessel and respond to inflammation)?
blood vessel in tissue - venules
• lined by endothelial cells with receptors
• inside venule are blood cells- monocytes & neutrophils
So cytokines bind to receptors on endothelial lining of blood vessel, cause induction (increased expression) of molecules on luminal side which are the adhesion molecules
• adhesion molecules - promote sticking of cells - so Blood cells stick to them which is first step in getting them out of vessel
• E- selectin (adhesion molecule on luminal wall) and neutrophil has adhesion molecules on surface (E selectin ligand) low affinity interaction
• cells make these low affinity interactions as it flows down vessel
• then ICAM-1 on endothelial binds to integrin (LFA-1) on neutrophil - a high affinity interaction, neutrophil stops slowly (stable arrest) flattens out then squeezes to get out of blood vessel to go fight infection in tissue, phagocytosis- apoptosis
• now there is a lot of dead apoptotic neutrophils in tissue
Monocytes go thru same process into the tissue - change to macrophages in tissue
* they eat the microbes and neutrophils there (clean up process)
what is stable arrest in inflammation?
stable arrest is the high affinity interaciton made between neutrophils/monocyte in the blood and surface molecules
* ICAM-1 on endothelium binds to integrin LFA-1 on neutrophils
then neutrophil/monocyte stops in its path, flattens out, and squeezes into the tissue to go fight and phagotyosize
what are the adhesion molecules that create low affinity interactions?
E-selectin on luminal wall
E selectin ligand on neutrophil/monocyte
describe the formation of PUS in inflammation? and the components that make up PUS
neutrophils die for us so that we could live *** formation of PUS
microbes multiple in tissue
cytokines build up, increase blood flow, and cause inside of endothelium to become sticky
neutrophils cumulate in large numbers around microbe then apoptosis
fluid & components of apoptotic neutrophils form pus
components of PUS:
• DNA from neutrophils
• bacteria killed by neutrophils
• apoptotic neutrophils
what is psoriasis? and how is it related to inflammation? what is the treatment?
psoriasis is an inflammatory skin disease that triggers an inflammatory response towards self
* autoimmune
* can cause arthritis (inflammation of joints)
• psoriasis lesions are filled with immune cell infiltrate (leukocytes accumulate in skin)
treatment:
biologics - target TNFα (cytokine) which blocks interaction with the TNFα receptor to adhesion molecule
(TNFα – A pro-inflammatory cytokine, often released by macrophages and dendritic cells early in acute inflammation)
• drug prevents expression of adhesion molecules on surface of endothelial cells, prevents leukocytes from entering tissue AND drug prevents TNFα from acting directly on skin cells, blocking overall skin growth
• side effects of not having an inflammatory response (protects us from infection) - suppressing someones immune system with this drug we put ppl at risk for infection, make sure patients immune systems are good (vaccines etc)
• drug alters your immune function
Small leukocytes that are central players in the adaptive immune system. Lymphocytes include T cells and B cells.
lymphocytes
