Pathology Test 4 Immunity

Front 1

What are the main parts of the innate immune system?

Back 1

skin
phagocytes
NK cells
complement
Toll like receptors- (stimulate innate immune response)

Front 2

What cell controls cell mediated adaptive immunity?

Back 2

T-lymphocytes

Front 3

What cell controls humoral adaptive immunity?

Back 3

B cells- produce antibodies

Front 4

How do T cells recognize cell bound antigen?

Back 4

They used a TCR or T cell receptor

Front 5

What makes up the TCR, and what is is complexed with?

Back 5

This has a variable (antigen binding region)

the constant region- has CD3 and Xi chain dimer (funny E).
Used for signal transduction, NOT binding

Front 6

What is the usefulness of TCR gene rearrangments

Back 6

used as a molecular marker of T-lineage cells

used to classify lymphoid malignancies

Front 7

What do CD4 cells bind to?

Back 7

Class 2 MHC's

Front 8

What do CD4+ cells do?

Back 8

these are helper cells, they secrete cytokines that influence other cells

Front 9

What do TH1 cells secrete?

Back 9

IL-2, IFN- involved in cell mediated immunity

Front 10

What do TH2 cells secrete?

Back 10

IL-4, and IL-5, used in humoral immunity

Front 11

What do CD8+ cells bind to?

Back 11

MHC class 1

Front 12

What do CD8+ cells do?

Back 12

these are cytotoxic cells, kill infected cells directly

Front 13

What are the two signals a T cell needs for activation?

Back 13

TCR (CD+MHC)

and CD28 + costimulatory molecule on MHC

Front 14

What do B cells become when stimulated by antigen?

Back 14

these become plasma cells

Front 15

What is the antigen binding component on B cells

Back 15

Surface IgM or IgD are used for antigen binding

Front 16

What is the usefulness of rearranged IG genes on B cells?

Back 16

This is used as a molecular marker for B cells

Front 17

What are the two types of dendritic cells, and what do they do?

Back 17

Interdigitating dendritic cells (Langerhans cells)- Used for antigen presenting in primary immune responses

Folicular dendritic cells- found in germinal centers of lymphoid follicles-
These have Fc receptor for IgG, trap antigen bound to antibody

Front 18

What is the innate ability of NK cells?

Back 18

these can lyse tumor and infected cells without prior stimulation

Front 19

What are the CD markers of NK cells?

Back 19

16 and 56

Front 20

What does CD16 do? and what is ADCC?

Back 20

this is a Fc receptor for IgG
Allows NK cells to lyse IgG coated target cells--this is called ADCC (antibody dependent cell mediated cytotoxicity)

Front 21

What are the two receptors on NK cell membranes and what do they do?

Back 21

theres a inhibitor which binds normal class 1 MHC's

and there is a killing one, turned on by some molecule on target cell

Front 22

What do NK cells secrete?

Back 22

cytokines

Front 23

What are MHC complexes used for?

Back 23

peptide antigen presentation

Front 24

What chromosome are MHCs from?

Back 24

chromosome 6
called MHC or HLA gene cluster

Front 25

What are the three categories of the HLA system?

Back 25

Class 1- coded by A,B,C.- presents on all nucleated cells- displays abnormal peptides

Class 2- coded by D- only found on monocytes, macrophages, dendritic cells, and B cells

Class 3- some of the complement components

Front 26

What is the best known disease assocaited with HLA?

Back 26

ankylosing spondylitis

Front 27

What are the three categories of HLA associated diseases?

Back 27

Inflammatory diseases (ankylosing spondylitis)

Inherited erros of metabolism

Autoimmune diseases

Front 28

What is a type I hypersensitivity?

Back 28

immediate anaphylactic rxn due to IgE

Front 29

What is a type II hypersensitivity?

Back 29

Antibody mediated (usually cross reaction)

Front 30

What is a type III hypersensitivity?

Back 30

immune complex mediated- body produces antibodies and complement that deposit into joints and tissues, causing inflammation

Front 31

What is a type IV hypersensitivity?

Back 31

cell mediated hypersensitivity
activate T cells

Front 32

What T cells are activated in a type 1 hypersensitivity?

Back 32

Th2 cells- secretes IL-4 - this causes IgE secretion from B cells

and IL-5- activates eosinophils

Front 33

What is the chain of events in a type 1 hypersensitivity rxn?

Back 33

Mast cells are sensitized by IgE antibody

The mast cells are activated and release mediators upon exposure to antigen (activated by IgE cross linking)

Front 34

What are the immediate responses of a type 1 hypersensitivity rxn?

Back 34

Vasodilation
Vascular Leakage
Smooth muscle spasm
(5-30 min)

Front 35

What is the late phase reaction of a type 1 hypersensitivity rxn?

Back 35

2-8 hours later
inflammation, tissue destruction

Front 36

What cell is important in late phase of type 1 hypersensitivity rxns?

Back 36

Eosinophils- these contain many mediators that are responsible for many symptoms

Front 37

What is Atopy?

Back 37

a predisposition to develop hypersensitivity reactions to inhaled agents

Front 38

What are the three effector mechanisms of antibody mediated injury in type II hypersensitivity rxns?

Back 38

Opsonization and phagocytosis

Inflammation

antibody mediated cellular dysfunction

Front 39

What are the four clinical situations in which opsonization and phagocytosis occur? (in type II hypersensitivity rxns)

Back 39

Transfusion reactions

erythroblastosis fetalis

Autoimmune hemolytic anemia, agranulocytosis, thrombocytopenia

some drugs (penicillin)

Front 40

What two diseases are examples of antibody mediated cellular dysfunction?

Back 40

Myasethnia gravis- with antibodies inhibiting the NMJ

Graves disease- with antibodies stimulating the thyroid

Front 41

What type types of antigens can cause immune complex injury in type III hypersensitivity rxns?

Back 41

Exogenous (foreign protein, bacteria, viruses)

Endogenous- self antibodies against self

Front 42

What are the two patterns of injury seen in type III hypersensitivity rxns?

Back 42

Circulating immune complexes (antigen combines with antibody in circulation, deposed in vessel walls)- called Generalized*


In situ immune complexes (complexes form at extravascular sites, where antigen may have been deposited before)- Localized**

Front 43

What are the three phases of the systemic form of type III hypersensitivity rxns?

Back 43

Immune complex formation

immune complex deposition (small ones circulate longer, large one removed by MPS system- can be overwhelmed)

inflammation rxn @ sites of deposition- about 10 days after antigen administration

Front 44

What is the major morphologic feature of immune complex injury?

Back 44

tissue injury usually occurs in kidneys, joints, and small vessels.

Acute necrotizing vasculitis
(fibrinoid necrosis in vessel walls)

10 days after administration of the antigen, causes fever, arthalgias, urticaria, lymph node enlargement, complement, neutrophil and macrophage activation

Front 45

What are the two types of reactions of type IV hypersensitivity rxns? and what cells causes each?

Back 45

Delayed type hypersensitivity rxns, with CD4 cells

and Direct cell cytotoxicity with CD8 cells

Front 46

What is the classic example of delayed type IV hypersensitivity?

Back 46

Mantoux reactions (the TB test). CD4 cells cause this

which is elicited in people already sensitized to tubercle bacillus by previous infection

Front 47

How does a delayed type hypersensitivity rxn occur?

Back 47

Niave CD4 cells recognize an antigen in a class II MHC.
-this produces effector and memory CD4 cells of TH1 type.

APC's produce IL-12 which turns on Th1 type T cells.

NK cells and Th1 produce INFy- which activates macrophages

turns into a feedback loop

Front 48

What are the two hypersensitivity types in transplant rejection

Back 48

cell mediated and antibody mediated

Front 49

How are grafts directly rejected?

Back 49

T cells recognize graft MHC complexes.

CD4 helper cells triggered by class II MHC's on grafts

CD8's recognize class I MHC's and kill them

Front 50

How are grafts indirectly rejected?

Back 50

CD4+ cells recognize donor MHC molecules after APC's bring them in.

this causes antibody production

Front 51

What is hyperactue rejection?

Back 51

the body already has preformed antibodies to the donors tissues - causes ischemic death of graft

Front 52

what is acute graft rejection?

Back 52

days to weeks (but can be held off for months)

by either cellular or humoral methods
humoral causes rejection vasculitis

Front 53

What are the signs of chronic graft rejection?

Back 53

months to years later,
you see vascular changes, interstitial fibrosis, and loss of parenchyma

immunosuppression will not help

Front 54

How do you increase graft survival?

Back 54

HLA matching, and immunosuppression therapy

Front 55

What are the three complications of Allogenic hematopoietic stem cell transplants?

Back 55

transplant rejection
graft verses host disease
immune deficiencies

Front 56

What mediates transplant rejection in allogenic hematopoeitc stem cell transplants?

Back 56

Mediated by radiation resistant T-cell, and NK cells in the host

Front 57

What three organs are target in GVH disease?

Back 57

liver, skin, and gut

Front 58

How does GVH disease happen?

Back 58

you transplant immune competent cells into an immune compromised pt.

the T cells from the donor react to their new surroundings