Immunology L2R

Question 1

What are levels of innate Immunity?

Answer 1

Levels of Innate Immunity

Barriers: Physical,chemical,microbial

Molecular: Complement, Anitmicrobial Peptides, Antimicrobial Enzymes

Cellular: Natural Killer Cell, Macrophages and monocytes, Dendritic cell, Neutrophil

Question 2

Explain physical barriers and Label Barriers in the Mucosal Surfaces.

Answer 2

1. Strong Physical Barriers : Skin, Hair, Nails
2. Vulnerable Barrier: Mucosal membrane
   - Barriers at Mucosal Surfaces Physical& Chemical

Question 3

what are the specific defenses regarding Skin, Gut, Lungs, and Eyes?

Answer 3

see pictue

Question 4

What are the Molecular Defenses and there specific tasks?

Answer 4

1. Antimirobial Peptides
2. Complements
3. antimiborbial Enzymes

Question 5

what are the pathways that will end up making a complement?

Answer 5

Pathways that lead to terminal complement are

1. Alternative Pathway: when a pathogen is detected blood protien sill bend to the surface and converge at C3 Convertase.

2.Classical Pathway: its part of the adaptive immunity system, detects microbe by marking them with antibodies which complent binds to antibodies also become C3 Convertase

3.The Lectin Pathway: binding of lecin to mannose on surface of pathogen which goes to C3 convertase.

Question 6

what are the 3 molecular defenses and there function?

Answer 6

Antimicrobial Enzymes: Lysozyme breaks down peptidoglycan (like pac__-man), exposing the bacterial membrane

Antimicrobial peptides: Amphipathic ( having a hydrophilic and hydrophobic side)

1. Defensins are brought to lipid layer b/c of amphipathic properties
2. Form a pore.

Antimicrobial Molecules: in the gut epithelium, Paneth cells produce antimicrobial proteins: Alpha-defensins and lectin Reglll.

Question 7

List the Cellular defenses and their functions.

Answer 7

1. Neutrophil: short-lived phagocyte, Kamikaze cells, granules
   - Most abundant white blood cells in circulation

Process:

• Multi-lobe nucleus allows migration through tight spaces.
• changes shape to become amoeba-like w/pseudopods to hunt microbes
• Uses chemokine receptors and cytokine to follow where the battle is. (Marco-POLO)
• Kills through phagocytosis.
• Last resort they THROW THERE NUCLEUS.
  1. Natural Killer cell: Hold me back bro!!! Causes apoptosis to cells that have been infected, granules
• can kill an infected cell or a damaged cell. ( looks for cells with a lot of activating signals)
  1. Macrophages & Monocytes: Clean dead cells long-lived Phagocyte, reactive to Oxygen and Nitrogen Species.

Process

*Macrophages have receptors that bind to microbe and take it into a cell (phagosomes) microbe meets Lysosome. ( phagolysosomes ) :0 Leads to inflammation.

* for more evolved pathogens a 2nd signal is given in the phagolysosomes state, releasing oxygen radicals which disrupt membrane.

*Uses NADPH to form radicals

Monocytes: in blood after the sign of infection will matue to macrophages (preferred) or dendritic cells.

1. Dendritic cells: ( runs to Lymph nodes ), a bridge between innate and adaptive. travel form periphery(site of infection ) to the lymph nodes via the lymphatics

Question 8

What is PRRs and PAMPs?

Answer 8

PRRs recognize PAMPS ( pathogen-associated molecular patterns) but also host cells that have been damaged by.

Question 9

what are Type I Interferon’s?

Answer 9

Type I Interferon: (FIRE ALARM OF CELL)

-When the infection is detected by PRRs in the cell, the cell makes IFN

It sends out the IFN and other cells receive the signal by receptor ( helps them to resist infection ) and then respond, meanwhile the cell shutdown and goes into an antiviral state.

side note: NF-kB leads to inflammation, and stimulation of adaptive immune system.

Question 10

Answer 10

see the other side