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PCB4233: Immunology. Dr. Mauricio Rodriguez-Lanetty Email: [email protected] Phone: 305-3484922 Lecture 3. On January 18 th , the lectures will be uploaded to Blackboard Learn On January 21 st , a question-based guide covering the first four lectures will be provided. Skin. Interactions:.

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pcb4233 immunology

PCB4233: Immunology

Dr. Mauricio Rodriguez-Lanetty

Email: [email protected]

Phone: 305-3484922

Lecture 3

slide2

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

slide3

Skin

Interactions:

consequences:

Blood vessel

slide4

Skin

Interactions:

consequences:

Macrophage

Blood vessel

slide5

Skin

Interactions:

consequences:

PRR-PAMP

Macrophage

Blood vessel

slide6

Skin

Interactions:

consequences:

PRR-PAMP

1) Phagocytosis of the pathogen

2) Cell signaling that trigger expression of cytokines and chemokines

Blood vessel

slide7

Skin

Interactions:

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

slide8

Skin

Interactions:

consequences:

PRR-PAMP

1) Phagocytosis of the pathogen

2) Cell signaling that trigger expression of cytokines and chemokines

Blood vessel

TLR4

CD14

Cell membrane

Toll-like receptor signaling pathway

slide9

Skin

Interactions:

consequences:

PRR-PAMP

1) Phagocytosis of the pathogen

2) Cell signaling that trigger expression of cytokines and chemokines

Bacteria

Blood vessel

LPS

TLR4

CD14

Cell membrane

slide10

Skin

Interactions:

consequences:

PRR-PAMP

1) Phagocytosis of the pathogen

2) Cell signaling that trigger expression of cytokines and chemokines

Bacteria

Blood vessel

LPS

TLR4

CD14

Cell membrane

Activation of

transcription

factors (NF-kB)

Stimulation of gene

expression

Cytokines

(TNF-α, IL-1, CXCL8)

Inflammation,

migration of

leukocytes,

adaptive immunity

slide11

Skin

Interactions:

consequences:

PRR-PAMP

1) Phagocytosis of the pathogen

2) Cell signaling that trigger expression of cytokines and chemokines

Cytokines

Blood vessel

slide12

Skin

Interactions:

consequences:

PRR-PAMP

1) Phagocytosis of the pathogen

2) Cell signaling that trigger expression of cytokines and chemokines

Cytokines

Blood vessel

Cytokines – blood vessel endothelia cells

slide13

Skin

Interactions:

consequences:

PRR-PAMP

1) Phagocytosis of the pathogen

2) Cell signaling that trigger expression of cytokines and chemokines

Cytokines

Blood vessel

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

slide14

Skin

Interactions:

consequences:

PRR-PAMP

1) Phagocytosis of the pathogen

2) Cell signaling that trigger expression of cytokines and chemokines

Chemokines

Cytokines

Blood vessel

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 – Leukocytes

CXC8 or IL-8

slide15

Skin

Interactions:

consequences:

PRR-PAMP

1) Phagocytosis of the pathogen

2) Cell signaling that trigger expression of cytokines and chemokines

Chemokines

Cytokines

Blood vessel

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 – Leukocytes

CXC8 or IL-8

5) Induce chemotaxis

6) Help in the adhesion of phagocyte during migration

slide16

Skin

Interactions:

consequences:

PRR-PAMP

1) Phagocytosis of the pathogen

2) Cell signaling that trigger expression of cytokines and chemokines

Chemokines

Cytokines

Blood vessel

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 – Leukocytes

CXC8 or IL-8

slide17

Skin

Blood vessel

Who are the first to migrate to the site of infection?

slide18

Skin

Neutrophils

Blood vessel

Do neutrophils look (morphological) similar to macrophages?

slide19

Skin

Neutrophils

Blood vessel

slide20

Skin

Neutrophils

Blood vessel

How they kill the pathogens especially bacteria?

slide22

Once ingested: inside the phago-lysosome

The respiratory burst in macrophages and neutrophils is caused by a transient increase in oxygen consumption during the production of microbicidal oxygen metabolites

This occur both in macrophages and neutrophils

slide23

How important is this Respiratory burst to clear infections?

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

slide24

Skin

Neutrophils

Blood vessel

How they kill the pathogens especially bacteria?

Phagocytosis

Respiratory burst (a production of a buch nasty reactive oxygen species that kill bacteria)

slide25

Skin

Blood vessel

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

slide26

Skin

Neutrophils

Blood vessel

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?

slide27

Skin

Blood vessel

  • 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-phagocytic

Killer]

slide28

Skin

How they distinguish an infected from a healthy, uninfected cell?

Blood vessel

  • 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-phagocytic

Killer]

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