MIP 342 Lecture Notes - Antigen Processing, Tlr 1, Neutrophil

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lemondog142

11 Jul 2014

School

CSU

Department

Microbio, Immun, Pathology

Course

MIP 342

Professor

Alan Schenkel

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Document Summary

Only 3 types of immune cells can activate na ve t cells. B cells mostly when antigen levels are low. Toll-like receptors (means a pathogen is present) prrs (pattern recognition receptors), bind to a pamp (pathogen associated molecular pattern) on a pathogen. Tissue damage cause release of immune mediators. Not good at presenting antigen (low levels of mhc and co-stimulatory molecules) As the activated dc migrates to the ln, it changes from a cell that was once good at phagocytosing antigen into one that is now superior at presenting antigen to na ve t cells. Ccr7 on dc (directs to lymph nodes) Ccr7 signaling co-stimulatory molecules (b7. 1, b7. 2, members of immunoglobulin superfamily) 3 signals drive clonal expansion and differentiation of na ve t cells. Ligation of b7 on apc with cd28 on t cell signals up-regulation of il2/il2r proliferation. Ctla-4 looks similar to cd28 inhibits t cell. Review it"s important that only activated apcs can prime na ve t cells.

Related Questions

1. Macrophages express multiple types of receptors on their surface that stimulate phagocytosis of microbes, leading to pathogen internalization and destruction. Many of these receptors, such as Dectin-1, rely on direct recognition of a PAMP on the pathogen surface. However, some receptors that stimulate phagocytosis rely on soluble factors (not associated with the phagocyte membrane) to identify and mark the pathogen for uptake by the phagocyte. One such receptor is:

		a) The class A scavenger receptor
		b) The complement receptor
		c) The mannose receptor
		d) The macrophage C-type lectin receptor
		e) The lipid receptor

2. Toll-like receptor (TLR) signaling pathways lead to the activation of NFkB and of IRF family transcription factors. Each pathway has multiple steps, beginning with adapter proteins in various combinations. This process will induce inflammatory cytokine gene expression rapidly. The following are such adapter proteins EXCEPT:

a) MyD88

b) MAL

c) TRIF

d) NFkB

e)TRAM

3. Many of the inflammatory mediators produced by tissue macrophages at sites of infection act on the endothelial cells lining the blood vessel walls. An exception to this is (are) the:

		a) Cytokines that induce increased vascular permeability
		b) TNF produced by tissue-resident sensor cells
		c) Bradykinin produced that causes pain
		d) Chemokines that induce directed migration of blood monocytes
		e) Cytokines that induce increased expression of adhesion molecules

apricotfish623

Which of the following is a characteristic of the adaptive immune system?

a .It is a specific response against microbial antigen

b. It includes inflammation.

c. It activates the alternative complement pathway.

d. It includes defenses on the body surfaces.

2. C-reactive protein is an opsonin because it:

a. creates a channel in bacterial membranes

b. increases C3b binding to a microbe.

c. forms the pathogen-associated molecular patterns.

d. enhances phagocytosis.

3. The rapid increase in antibody production after repeated exposures to the same antigen is due to:

a. antibody-dependent cellular cytotoxicity.

b. higher levels of IgE

c. presence of memory cells.

d. clonal proliferation of NK cells

4. Cytotoxic T cells can kill cancer cells by:

a. inducing apoptosis with granzyme.b. release of membrane attack complex.

c. activate the production of complement C3b

d. phagocytosis of opsonized cells.

5. Which event is not required for the activation of helper T cells?

a. The presence of interleukin-1

b. Binding of CD8 receptors

c. Binding of matching non-antigenic proteins of the antigen-presenting cel

d. Presentation of an antigen bound to class II MHC

plumworm266

1. C-reactive protein is an opsonin because it:

a. creates a channel in bacterial membranes

b. increases C3b binding to a microbe.

c. forms the pathogen-associated molecular patterns.

d. enhances phagocytosis.

2. The rapid increase in antibody production after repeated exposures to the same antigen is due to:

a. antibody-dependent cellular cytotoxicity.

b. higher levels of IgE

c. presence of memory cells.

d. clonal proliferation of NK cells

3. Cytotoxic T cells can kill cancer cells by:

a. inducing apoptosis with granzyme.b. release of membrane attack complex.

c. activate the production of complement C3b

d. phagocytosis of opsonized cells.

4. Which event is not required for the activation of helper T cells?

a. The presence of interleukin-1

b. Binding of CD8 receptors

c. Binding of matching non-antigenic proteins of the antigen-presenting cel

d. Presentation of an antigen bound to class II MHC

PLEASE DO NOT ANSWER IF YOURE NOT WILLING TO ANSWER ALL PARTS. Ive already finished this, I am trying to compare answers

byzantiumhedgehog137

MIP 342 Lecture Notes - Antigen Processing, Tlr 1, Neutrophil

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