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PCB4233: Immunology Dr. Mauricio Rodriguez-Lanetty Phone: 305-3484922 Lecture 3.

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Presentation on theme: "PCB4233: Immunology Dr. Mauricio Rodriguez-Lanetty Phone: 305-3484922 Lecture 3."— Presentation transcript:

1 PCB4233: Immunology Dr. Mauricio Rodriguez-Lanetty Phone: Lecture 3

2 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

3 Blood vessel Skin Interactions:consequences:

4 Blood vessel Skin Interactions:consequences: Macrophage

5 Blood vessel Skin Interactions:consequences: PRR-PAMP Macrophage

6 Blood vessel Skin Interactions:consequences: PRR-PAMP1) Phagocytosis of the pathogen 2) Cell signaling that trigger expression of cytokines and chemokines

7 Blood vessel Skin Interactions:consequences: PRR-PAMP1) Phagocytosis of the pathogen 2) Cell signaling that trigger expression of cytokines and chemokines A well known example of this!

8 Blood vessel Skin Interactions:consequences: PRR-PAMP1) Phagocytosis of the pathogen 2) Cell signaling that trigger expression of cytokines and chemokines Cell membrane CD14 TLR4 Toll-like receptor signaling pathway

9 Blood vessel Skin Interactions:consequences: PRR-PAMP1) Phagocytosis of the pathogen 2) Cell signaling that trigger expression of cytokines and chemokines Cell membrane Bacteria LPS CD14 TLR4

10 Blood vessel Skin Interactions:consequences: PRR-PAMP1) 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

11 Blood vessel Skin Interactions:consequences: PRR-PAMP1) Phagocytosis of the pathogen 2) Cell signaling that trigger expression of cytokines and chemokines Cytokines

12 Blood vessel Skin Interactions:consequences: PRR-PAMP1) Phagocytosis of the pathogen 2) Cell signaling that trigger expression of cytokines and chemokines Cytokines Cytokines – blood vessel endothelia cells

13 Blood vessel Skin Interactions:consequences: PRR-PAMP1) Phagocytosis of the pathogen 2) Cell signaling that trigger expression of cytokines and chemokines Cytokines Cytokines – blood vessel endothelia cells TNF-α3) Activate endothelia cells. So more adhesion molecules are expressed, like selectins and ICAMS 4) Vasodilation and increase vascular permeability

14 Blood vessel Skin Interactions:consequences: PRR-PAMP1) Phagocytosis of the pathogen 2) Cell signaling that trigger expression of cytokines and chemokines Cytokines Cytokines – blood vessel endothelia cells TNF-α3) 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

15 Blood vessel Skin Interactions:consequences: PRR-PAMP1) Phagocytosis of the pathogen 2) Cell signaling that trigger expression of cytokines and chemokines Cytokines Cytokines – blood vessel endothelia cells TNF-α3) 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 chemotaxis 6) Help in the adhesion of phagocyte during migration

16 Blood vessel Skin Interactions:consequences: PRR-PAMP1) Phagocytosis of the pathogen 2) Cell signaling that trigger expression of cytokines and chemokines Cytokines Cytokines – blood vessel endothelia cells TNF-α3) 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

17 Blood vessel Skin Who are the first to migrate to the site of infection?

18 Blood vessel Skin Neutrophils Do neutrophils look (morphological) similar to macrophages?

19 Blood vessel Skin Neutrophils

20 Blood vessel Skin Neutrophils How they kill the pathogens especially bacteria?

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22 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

23 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?

24 Blood vessel Skin Neutrophils How they kill the pathogens especially bacteria? PhagocytosisRespiratory burst (a production of a buch nasty reactive oxygen species that kill bacteria)

25 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

26 Blood vessel Skin Neutrophils How they kill the pathogens especially bacteria? PhagocytosisRespiratory burst (a production of a buch nasty reactive oxygen species that kill bacteria) So, do all leukocytes kill through phagocytosis?

27 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-phagocytic Killer]

28 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-phagocytic Killer] How they distinguish an infected from a healthy, uninfected cell?

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