pcb4233: immunology dr. mauricio rodriguez-lanetty email: rodmauri@fiu.edu phone: 305-3484922...
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PCB4233: Immunology
Dr. Mauricio Rodriguez-LanettyEmail: rodmauri@fiu.edu
Phone: 305-3484922
Lecture 3
On January 18th, the lectures will be uploaded to Blackboard Learn
On January 21st, a question-based guide covering the first four lectures will be provided
Blood vessel
SkinInteractions: consequences:
Blood vessel
SkinInteractions: consequences:
Macrophage
Blood vessel
SkinInteractions: consequences:
PRR-PAMP
Macrophage
Blood vessel
SkinInteractions: consequences:
PRR-PAMP 1) Phagocytosis of the pathogen
2) Cell signaling that trigger
expression of cytokines and chemokines
Blood vessel
SkinInteractions: consequences:
PRR-PAMP 1) Phagocytosis of the pathogen
2) Cell signaling that trigger
expression of cytokines and chemokines
A well known example of
this!
Blood vessel
SkinInteractions: consequences:
PRR-PAMP 1) Phagocytosis of the pathogen
2) Cell signaling that trigger
expression of cytokines and chemokines
Cell membrane
CD14 TLR4
Toll-like receptor signaling pathway
Blood vessel
SkinInteractions: consequences:
PRR-PAMP 1) Phagocytosis of the pathogen
2) Cell signaling that trigger
expression of cytokines and chemokines
Cell membrane
Bacteria
LPS
CD14 TLR4
Blood vessel
SkinInteractions: consequences:
PRR-PAMP 1) Phagocytosis of the pathogen
2) Cell signaling that trigger
expression of cytokines and chemokines
Activation of transcription
factors (NF-kB)
Stimulation of gene expression
Cytokines (TNF-α, IL-1, CXCL8)
Inflammation, migration of leukocytes,
adaptive immunity
Cell membrane
Bacteria
LPS
CD14 TLR4
Blood vessel
SkinInteractions: consequences:
PRR-PAMP 1) Phagocytosis of the pathogen
2) Cell signaling that trigger
expression of cytokines and chemokines
Cytokines
Blood vessel
SkinInteractions: consequences:
PRR-PAMP 1) Phagocytosis of the pathogen
2) Cell signaling that trigger
expression of cytokines and chemokines
Cytokines
Cytokines – blood vessel
endothelia cells
Blood vessel
SkinInteractions: consequences:
PRR-PAMP 1) Phagocytosis of the pathogen
2) Cell signaling that trigger
expression of cytokines and chemokines
Cytokines
Cytokines – blood vessel
endothelia cells
TNF-α 3) Activate endothelia cells.
So more adhesion molecules are expressed, like selectins and
ICAMS
4) Vasodilation and increase
vascular permeability
Blood vessel
SkinInteractions: consequences:
PRR-PAMP 1) Phagocytosis of the pathogen
2) Cell signaling that trigger
expression of cytokines and chemokines
Cytokines
Cytokines – blood vessel
endothelia cells
TNF-α 3) Activate endothelia cells.
So more adhesion molecules are expressed, like selectins and
ICAMS
4) Vasodilation and increase
vascular permeability
Chemokines
Chemokines – Leukocytes
CXC8 or IL-8
Blood vessel
SkinInteractions: consequences:
PRR-PAMP 1) Phagocytosis of the pathogen
2) Cell signaling that trigger
expression of cytokines and chemokines
Cytokines
Cytokines – blood vessel
endothelia cells
TNF-α 3) Activate endothelia cells.
So more adhesion molecules are expressed, like selectins and
ICAMS
4) Vasodilation and increase
vascular permeability
Chemokines
Chemokines – Leukocytes
CXC8 or IL-8
5) Induce chemotaxis6) Help in the adhesion of phagocyte during migration
Blood vessel
SkinInteractions: consequences:
PRR-PAMP 1) Phagocytosis of the pathogen
2) Cell signaling that trigger
expression of cytokines and chemokines
Cytokines
Cytokines – blood vessel
endothelia cells
TNF-α 3) Activate endothelia cells.
So more adhesion molecules are expressed, like selectins and
ICAMS
4) Vasodilation and increase
vascular permeability
Chemokines
Chemokines – Leukocytes
CXC8 or IL-8
Blood vessel
Skin
Who are the first to migrate to the site of infection?
Blood vessel
Skin
Neutrophils
Do neutrophils look (morphological) similar to macrophages?
Blood vessel
Skin
Neutrophils
Blood vessel
Skin
Neutrophils
How they kill the pathogens especially bacteria?
The respiratory burst in macrophages and neutrophils is caused by a transient increase in oxygen consumption during the production of microbicidal oxygen metabolites
Once ingested: inside the phago-lysosome
This occur both in macrophages and neutrophils
Chronic Granulomatous Disease: a genetic deficiency of NADPH oxidase, so the phagocytes do not produce toxic oxygen species.
People with this disease are susceptible to bacterial and fungal infections
How important is this Respiratory burst to clear infections?
Blood vessel
Skin
Neutrophils
How they kill the pathogens especially bacteria?
Phagocytosis Respiratory burst (a production of a buch nasty reactive oxygen species that kill bacteria)
Blood vessel
Skin
Interferon (another cytokine) induced by viral infection:
Interferon induce a state of resistance to viral replication in all cells
IFN-α and IFN-β induce the expression of proteins that help to inhibit viral replication
Autocrine and paracrine effect
Activate dentritic cells and macrophage
Blood vessel
Skin
Neutrophils
How they kill the pathogens especially bacteria?
Phagocytosis Respiratory burst (a production of a buch nasty reactive oxygen species that kill bacteria)
So, do all leukocytes kill through phagocytosis?
Blood vessel
Skin
•Natural killer cells are non-phagocytic and granular lymphocytes that kill abnormal (e.g., infected or malignant) host cells•They account for 5-10% of all lymphocytes in circulation•The lineage of origin is different to macrophages, mast cells and the other granulocytes
NK (natural killer) Cells
[Non-phagocyticKiller]
Blood vessel
Skin
•Natural killer cells are non-phagocytic and granular lymphocytes that kill abnormal (e.g., infected or malignant) host cells•They account for 5-10% of all lymphocytes in circulation•The lineage of origin is different to macrophages, mast cells and the other granulocytes
NK (natural killer) Cells
[Non-phagocyticKiller]
How they distinguish an infected from a healthy, uninfected cell?
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