Immunology Exam 1 Weeks 1-4

Front 1

What are the cascade of events that happens in the classical pathway of the complement system?

Back 1

1) C1q: Binds to the pathogens surface.

2) C1r: Cleaves C1s to activate protease.

3) C1s: Cleaves C4 and C2

4) C4: Cleaved into C4a and C4b

5) C4b binds to C2/ C4a is a mediator of inflammation.

6) C2 bound by C4b is cleaved by C1s to produce C3 a and C3 b ( binds to the surface of the pathogen).

7) C4b binds c5 for cleavage by C2a

8) C5a is released (powerful anaflotoxin) C5b binds with C678 forming the membrane attack complex.

9) C9 helps to wall off the pore created by the membrane attack complex

Front 2

What are the cascade of events that happens in the alternate pathway of the complement system?

Back 2

1) C3b is bound by the classical pathway to which factor b binds which is stabilized by factor P

2) Factor B cleaves many C3 molecules to C3a and C3b. Ramping up the response to the pathogen.

*special Notes*

-Factor I and H prevent this from happening to "self" cells.

- C3 can spontaneously become C3H2O which = C3b

Front 3

Evaluate the role of the fluid phase of the and membrane bound C3 in the activation of the complement.

Back 3

The fluid phase always for transport of factors in the alternative pathway as well as the classical pathway. fluid phase also allows C3 to become C3H2O spontaneously to help amp up the immune response.

Front 4

CR1

Back 4

Processes and Clears oponized immune complexes.

Front 5

CR2

Back 5

Activates B Cells

Front 6

CR3

Back 6

Pattern recognition

Front 7

CR4

Back 7

Induces the burst respiratory

Front 8

What is Anaphylactic shock? How is it induced by C3 and C5?

Back 8

Sever allergic reaction. It is caused by an over release of the anaphylatoxins C3a and C5a

Front 9

Zyomogen

Back 9

inactive protein precursor

Front 10

Macrophage

Back 10

phagocytosis and bacterialcidal mechanism

Front 11

Dendritic Cells

Back 11

Antigen uptake

Front 12

Neutrophil

Back 12

Phagocytosis and antibacterial mechanisms

Front 13

Eosinophil

Back 13

Kills antibody coated parasites

Front 14

Basophil

Back 14

Promotion of allergic response and parasitic immunity.

Front 15

Mast cell

Back 15

Release of granules containing histamine

Front 16

Innate Immunity

Back 16

- 1st line of defense against pathogens

Front 17

Adaptive Immunity

Back 17

- Takes a few days to kick in.

- "Remembers" pathogen patterns

Front 18

Targets of the innate immunity?

Back 18

- Require features for the life of said pathogen.

Ex) Lipopolysacharide, peptidoglycan, RNA, Oxidase activity, ect.

Front 19

How does a cell prevent being attacked by complement activation?

Back 19

1) Factor H competes with factor B to bind C3b; if it manages to bind, then the convertase is not formed.

2) Factor I that regulates complement activation by cleaving cell-bound or fluid phase C3b and C4b

3) C1 is controlled by a plasma serine proteinase inhibitor or serpin, the C1 inhibitor (C1INH). C1INH binds the active enzyme C1r:C1s, and causes it to dissociate from C1q, which remains bound to the pathogen.

Front 20

What are toll-like receptors and what role do they play in the immune response. Where are they most commonly found?

Back 20

Proteins that line the cell membranes of macrophages and cells that activate them in response to pathogens.

Front 21

How are toll like receptors similar to mannose binding lectin and ficolins?

Back 21

They all recognize forgein cell patterns. MBL bind specific carbs, ficolins bind specific patterns, and so do to toll like reciptors.

Front 22

Identify Phagocyctic luekyocytes.

Back 22

Macrophages, eosinhils and neutrophils

Front 23

Process of phagocytosis:

Back 23

Phagocytosis begins with the neutrophil or macrophage flowing around the pathogen and engulfing it so that it winds up enclosed in a phagosome (phagocytic vesicle). But this is only the first step, because the more challenging task of destroying the microorganisms remains. Indeed, some pathogens have special, effective mechanisms for frustrating this destruction step. The next step is the fusion of lysosomes with the phagosome. The result is called a phagolysosome. Lysosome are derived from the Golgi apparatus, much like secretion vesicles, but their contents are focused on destroying microorganisms

Front 24

Phagosome:

Back 24

Vacuole containing a phagocytized particle.

Front 25

Macropinocytosis

Back 25

a form of endocytosis that accompanies cell surface ruffling

Front 26

Phagolysome

Back 26

fusion of phagosome and lysome

Front 27

Conventional Dendrite cell:

Back 27

Uses Phagocytized cells to produce signals to activate T-cells

Front 28

Plasmacytoid Dendrite cells

Back 28

produce viral interferions

Front 29

Autocrine

Back 29

affects itself when secreted

Front 30

paracrine

Back 30

Affects adjacent cells when it is secreted

Front 31

endocrine

Back 31

Affects cells far away when secreted

Front 32

TNF-alpha

Back 32

a cytokine that causes the vascular endthilum to activate, increases vascular permiblilty, increases lymph fluid drainage and increases entry of cells to tissue.

induces fever, shock, and mobilizes metabolites

Front 33

IL-1

Back 33

a cytokine that causes the vascular endthilum to activate, destroys tissue, increases acess of effector cells.

induces fever and production of IL-6

Front 34

IL-6

Back 34

Increases lymphocyte production and antibody production

induces fever and acute phase protien products

Front 35

Chemotaxis

Back 35

The release of cytokines that attract leukocytes to the area they were released.

Front 36

What are the two major groups of chemokines

Back 36

CC: Two adjacent cysteine residues nears its terminus

CXC: 2 cysteine residues are seperated by on amino acid residue.

Both aid in luekyocyte migration

Front 37

1st responding luekocyte

Back 37

Nuetrophil

Front 38

Disseminated Coagulation

Back 38

Blood clotting in tiny vessels in entire body caused by septis

Front 39

Luekocytosis

Back 39

increase in production of luekocytes