Innate Immunity - Binder Flashcards

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1
Q

What does a pathogen have to do to cause an infection (first step)?

A

They must adhere to the epithelium at the infection site.

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2
Q

What are some innate barriers to infection?

A
  1. Tight junctions between epithelial cells.
  2. Chemical secretions and mucins to prevent adherence
  3. Cilia
  4. Normal Flora
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3
Q

Describe the recognition-response paradigm in immunity.

A

The response of the immune system, both innate and adaptive arms rely on the ability of the immune cells to recognize pathogens.

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4
Q

What is a pathogen-associate molecular pattern (PAMP)?

A

PAMPs are conserved features of pathogen groups that serve as recognition sites for innate immune cells. These patterns are absent or shielded in the host to prevent recognition of self.

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5
Q

What is a Pathogen Recognition Receptor?

A

PRRs bind PAMPs to initiate a response. Response can be release of cytokines, complement, phagocytosis, etc. Receptors are present on macrophages, neutrophils, DCs, can be secreted, or can be intracellular.

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6
Q

What are the cellular elements of the innate immune system?

A
  • Macrophages
  • Dendritic Cells
  • NK Cells
  • Eosinophils
  • Basophils
  • Neutrophils
  • Mast Cells
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7
Q

Where are macrophages and DCs found and what do they do?

A

Macrophages and DCs mature from monocytes and migrate to the tissues where they stay. Upon pathogen-pattern recognition, they will destroy pathogens without need for adaptive immunity and present antigens for T-cell recognition.

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8
Q

Where are neutrophils located?

A

Neutrophils are resident to the blood and only enter the tissues upon infection.

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9
Q

Describe the general phagocytic scheme.

A

Pattern recognition of pathogen by cell-surface receptors (mannose, scavenger, LPS (CD14) etc.) results in phagocytosis and initiation of inflammation and cytokine release. Pathogen is degraded and presented on MHC-II for T-cell activation.

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10
Q

Describe respiratory burst of macrophages.

A

Increase in oxygen consumption by macrophages. Oxygen will be converted to superoxide and H2O2 as a chemical toxin to pathogens or to form NO, a vasodilator and immune signaling molecule.

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11
Q

What are defensins?

A

A diverse group of small cationic antimicrobial peptides. They can assist with phagocytosis and form aggregates to disrupt pathogen membranes.

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12
Q

What are the effector mechanisms of innate immune cells?

A
  1. Phagocytosis
  2. Cytokine release
  3. Complement
  4. Respiratory burst
  5. Defensins
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13
Q

Describe the complement system

A

Soluble molecules circulating in blood that recognize and bind to pathogens and aid in opsonization and form membrane attack complexes.

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14
Q

PRR: Mannose-binding lectin (MBL)

A

Free protein in the blood that recognize certain carbohydrates specific to pathogens (by spacing). They opsonize pathogens and activate complement.

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15
Q

PRR: Macrophage Mannose Receptor (MMR)

A

Cell surface receptor of macrophages (CD206) that recognizes patterns similar to MBLs and acts directly as a phagocytic receptor.

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16
Q

PRR: Scavenger Receptors

A

Cell surface receptor (CD204) that recognizes acetylated LDLs and anionic polymers and facilitates phagocytosis. These molecules are shielded by sialic acid on host cells.

17
Q

PRR: fMLP Receptors

A

Recognize fMet-Leu-Phe, the start of many bacterial proteins. Facilitates cytokine release to induce innate response.

18
Q

PRR: Toll-like Receptors

A

Broad range of PRRs that initiate a response specific to the pathogen that it recognizes.

For example:
- dsRNA binding to Tlr3 leads to INF production against viruses
- LPS binding to Tlr4 leads to release of TNFa and INF which are antibacterial

19
Q

PRR: NOD proteins

A

Present in the cytosol and recognize certain microbial products

20
Q

What are the 3 sequential roles of inflammation?

A
  1. Deliver additional immune cells to site of infection
  2. Induce local blood clotting to restore barrier
  3. Tissue Repair
21
Q

Describe extravasation of neutrophils

A

Endothelial cells of inflamed blood vessels begin to increase expression of adhesion molecules. Neutrophils are engaged with weak interactions to cause rolling. Chemokines cause conformational changes of integrins on the neutrophil and subsequent strong adhesion to endothelial surface causing arrest. Neutrophils then migrate through endothelial cells to site of infection.

22
Q

What do NK cells do?

A

NK cells seek and destroy virally infected cells and secrete cytokines to direct other immune cells. Infected cells release TNFs which activate NK cells. Can kill lymphoid tumor cells without immunization.

23
Q

Describe the “surveillance” role of NK cells.

A

NK cells are thought to survey target cells for self molecules displayed on MHC-I. If self is recognized, the activating receptor on NK cells is over-ridden and no response is initiated. If however, the MHC-I is absent or altered, it cannot stimulate an inhibitory signal and the activation signal takes proceeds leading to NK cell facilitated apoptosis. Complex balance between inhibitory and activation signals.

24
Q

How do NK cells distinguish between virally infected cells and uninfected cells?

A

Infected cells secrete IFN alpha/beta and increase MHC-I expression.

25
Q

How do NK cells signal to the rest of the immune system upon activation?

A

Secretion of TNF alpha and INF gamma

26
Q

Which cells secrete IL-6?

A

Macrophages and dendritic cells, enhances responses

27
Q

Which cells secrete IL-1? What does it do?

A

Macrophages, enhances responses

28
Q

Which cells secrete CXCL8 (IL-8)? What does it do?

A

Phagocytes generally, chemoattractant for neutrophils

29
Q

Which cells secrete IL-12? Which cells does it act on?

A

Macrophages and dendritic cells, acts on naiive T-cells

30
Q

Which cells secrete TNF-alpha? Which cells does it act on?

A

Macrophages and DCs. Acts on epithelial cells to cause upregulation of adhesion molecules.