Immunology - Part 2 (For Midterm)

Front 1

Example of something that can cause type 1 , type 2, and type 4 hypersensitivity?

Back 1

penicillin:
T1: if ur allergic
T2: penicillin acts as hapten, binds to cell, and you attack ur own cell (autoimmune)
T4: if applied topically, again acts as hapten and binds skin proteins; Th1 get's pis sed off and releases cytokines to recruit CTLs

Front 2

During FIP infection (caused by feline corona virus), what determines type of disease animal gets (wet vs. dry form), and whether or not protective immunity develops?

Back 2

Determined by type of IMMUNE RESPONSE infected animal mounts
* with dry form, see mild Th1 response
* with wet form, see strong Th2 response, along with intense αB production
note: both forms are fatal

Front 3

IgG is in highest conc where?

Back 3

in blood

Front 4

Which Ab is dominant overall in blood?

Back 4

Often IgM, sometimes IgG

Front 5

Which Ab made during primary response to antigen? What does this mean diagnostically if present in high concentration?

Which Ab dominates secondary response?

Back 5

IgM, often indicates recent exposure

IgG

Front 6

Review question:

what are opsonins?

Back 6

proteins that promotes binding of pathogens to phagocytes

e.g. some αβ and complement protein act as opsonins

Front 7

In wet form of FIP why wud strong Th2 response (intense αB production) be problematic?

Back 7

* αB/Ag aggregations adhere to vessel walls
* complexes initiate hypersensitivity rxn or immune complex disease
* have inflammation and vasculitis, (vessels are leaky)
* high protein and cell.effusion into peritoneal cavity

Front 8

Review question:

Th2 secrete ?

Back 8

* Interleukin-4 and-5
stimulate B cell proliferation and antibody secretion… Thus, promote resistance to extracellular pathogens
*Think Humoral Immunity when you think of Th2 cells

Front 9

Pentanmeric Ab?

What Ab does not have Fc region?

Back 9

IgM

IgM (so will not help with opsinization!!!)

Front 10

Review question:

Th1 secrete?

Back 10

IL-2. Activates other T-cells, B cells and NK cells

* Interferon-y: also made by some other cells; activate macrophages primarily and thus promotes cell-mediated response.. Thus, promotes resistance to intracellular pathogens.
~Think CMI when you think of Th1 cells

Front 11

Which Ab's good at triggering complement?

Back 11

IgG, IgM <- best b/c have 5 Fc sites

CC does not get activated until these bind to antigen

Front 12

Review question:

Another name for CD8+ ?

Another name for CD4+ ?

Back 12

cytotoxic T cell

helper T cell

Front 13

Review question:

What binds Fc part of αβ?

Back 13

NK cells, macrophages, neutrophils <- cells of innate immune system have receptor for Fc part of ANTIBODY

(antibodies tag the antigen so these phagocytic can do their job)

Front 14

Review question:


structure of antibodies?

Back 14

identical to BCR from parent plasma B cell from which it is secreted, but enclosed in membrane,

2 light chains
2 heavy chains
variable region (attaches to antigen)
Fc region (attaches to cell e.g. neutrophil)

Front 15

Review question: (erase after midterm)
Endogenous antigen

Where made?
Processed by?
MHC molecule presented with?

Back 15

made by intracellular pathogen inside inf.host cell e.g. virus replicates and makes viral protein inside host cell expressing MHC-I

Inf. cell lysed cytotoxic T cell (CD8+)

Front 16

gamma globulin

Back 16

Most significant gamma globulins are immunoglobulins (Ig), aka αB, although some Ig's are not γ-globulins, and some γ-globulins are not Ig's.

Front 17

Which αB usually associated with mucosa?

Back 17

Secretory IgA

• Secretory component makes resistant to proteases of GI
• Major role is to bind antigen and prevent from binding epithelium – called “Immune exclusion”

note: serum IgA is monomeric

Front 18

How many Fc regions does IgA have?

Back 18

• Usually exists as a dimer (J-chain)

Front 19

Which species have placenta that allows passive transfer of IgG in utero?

Back 19

primate, dog, cat?

Front 20

Antibody-dependent-cell cytotoxicity (ADCC)

Back 20

The killing of antibody-coated target cells by cytotoxic cells (NK cells usually) with surface Fc receptors for the antibody.

Front 21

What can mediate lysis of cells, bacteria, viruses, parasites by binding to αB or directly to microrobes (w/o αB)?

Back 21

complement proteins

Front 22

What can facilitate phagocytosis via opsonization ?

Back 22

complement proteins

Front 23

What else can complement system do?

Back 23

* induce inflammation in tissue
* promote mast cell degran.
* clear immune complexes from circulation and deposits them in spleen and liver

Front 24

How do complement proteins induce inflammation in tissue?

Back 24

* chemotaxis of neutrophils,
* increase vascular permeability,
* induce contraction of smooth muscles

Front 25

What is the complement system?

Back 25

* Over 20 diff. proteins in blood
* No cells in the Complement System
* With infection, system of molecules is activated leading to sequence of events that ultimately targets surface of pathogens that help to destroy pathogen and eliminate infection.

Front 26

Which αB passes from breast tissue into milk (also found in tears, saliva, & bile)?

Back 26

secretory IgA, dimeric form

* Passes from breast tissue into milk to protect newborn
* also crosses mucosal surfaces (gut, urogenital tracts, respiratory for mucosal protection)

Front 27

How is complement system activated?

Back 27

Sequence of events referred to as “Complement Cascade”
“Alternate/Natural pathway” vs. Specific/Classical pathway

Front 28

Alternate/Natural pathway

Back 28

* CP activated (w/o αB), so this is example of innate immune response
* bind to microcrobes directly via C3

Front 29

Lectin Pathway

Back 29

* variation of "alternate pathway" group, again complement cascade activated w/o αB.

* lectin are glycoproteins on surface of microbes to which the complement proteins bind

Front 30

Specific Pathway

Back 30

* requires αB (IgG, IgM) to bind antigen before CC can be triggered
* When Ab is bound to pathogen, Fc region can activate CP (C1)
* this is example of specific immune response, so req. prior exposure or happens later in infection

Front 31

Which αB most efficient at triggering CC? Why?

Back 31

IgM b/c has 5 binding sites (Fc) for comp.protein.

(to have IgG activate CC need at least 2 IgG in close proximity)

Front 32

C1 binds to ? (be specific)

what must occur first?

Back 32

C1 (complement protein) binds to the constant heavy region or Fc portion of either IgM or IgG (subclasses) BUT only after antibody binds antigen!!

Front 33

two "forms" of IgM

Back 33

planar form (unbound)

staple form (bound Ag and waiting for C1 to come along)

Front 34

Next CP to bind after C1?
(in specific/active pthwy)

Back 34

C3

Front 35

What happens when complement cascade is activated?
(in specific/active pthwy)

*skip until know all other flashcards, because we don't have to memorize individual steps

Back 35

* binding of C1 (becomes enzymatic) allows binding of C3
* C3 bound to complex on pathogen surface
* C3 cleaved into C3b and C3a
* C3b also activates next step w/C5 blas and is a good opsonin (pro.phag)
* C3a (small peptide diffuses away and is a chemtacic factor
and promotes inflammation)

Front 36

What is different in Natural/Lectin/Alt. pathway?
(aside from lack of αB)

Back 36

C1 not involved, basically C3 binds directly to polysaccharides (e.g. lectin) of bacterial surface

Front 37

What happens when complement cascade is activated?

Back 37

* Just know that cascade continues and at some point a final complex forms on pathogen surface that causes cell lysis.
* This complex is called the Membrane Attack Complex (MAC)

Front 38

have anaphylatoxin activity, directly triggering degranulation of mast cells as well as increasing vascular permeability and smooth muscle contraction.

Back 38

Both C3a and C5a
(these are complement proteins)

Front 39

How do some bacteria develop resistance or evade the complement system?

Back 39

* Capsule prevents MAC insertion (Streptococcus)
* Capsule prevents C3b deposition (Streptococcus)
* Some bacteria possess ELASTASE that inactivates some complement components

Front 40

How do some viruses evade complement system?

Back 40

* Some viruses interrupt CC due to proteins that mimic regulatory proteins

Front 41

How do some tumor cells evade complement system?

Back 41

* Some tumor cells can endocytose MAC then seal up the membrane

Front 42

What are the Molecules that bind antigen?

Back 42

MHC
TCR
BCR
Antibody

Front 43

Two categories of mucosal lymphoid tissues:

Back 43

Inductive Sites

Effector Sites

Front 44

Inductive Sites

Back 44

Sites where Ag encountered and immune responses (humoral and CMI) are initiated.

Examples: Tonsils; Appendix; GALT; BALT; Peyer’s patches;

Front 45

Effector Sites

Back 45

Mucosal sites where αβ and cell-mediated responses are carried out… are doing their job (diffuse lymphoid tissues at mucosal surfaces).

Front 46

Why is it important to distinguish between Inductive Sites and Effector Sites?
(give example of their relationship)

Back 46

B/c some B cells may encounter antigen in GI tract, and then release αB in mammary glands (to be secreted into milk); so milk will have αB (primarly IgA inducted at mucosal surfaces) against intestinal Ag and microbes..important to new born.

Front 47

Where does IgA end up, after newborn has ingested it with milk?

Back 47

Unlike IgG (in colostrum) which is absorbed in blood stream, this IgA remains in GI to protect mucosal surface; this is good thing b/c IgA (mentioned in previous flashcard) is specific for intestinal microbes!

Front 48

what in meant by immune exclusion?

Back 48

IgA is particularly important in this
- prevents microbes or Ag from binding to mucosa

"prevent adherence of bacteria and viruses to epithelial surfaces"

Front 49

Where is IgA made?

How does it get to luminal surface?

Back 49

where ever plasma cells are like lymph node, *submucosal surface*

secreted from plasma cell as dimer (attached by J-chain), on submucosal surface have polyimmunoglobulin receptor binds IgA dimer, brings into epithelial cell via pinocytosis, shuttled to luminal surface, released in lumen of GI (still attached to polyiummunoglobulin receptor)

Front 50

What is meant by Secretory Piece?
What is function?

Back 50

* Part of the Poly-Ig receptor molecule is cleaved off leaving the receptor peptide chain still attached to the IgA.
* Receptor peptide chain is called the <>
* dimeric IgA now known as Secretory IgA and has resistance to proteases

Front 51

What is most important antibody in Immune Elimination? e.g. if it has infected enterocyte or adhered to mucosal lining?

Back 51

Mediated by IgE primarily…
(IgG to lesser extent)

If invading organisms evade IgA
and gain access to tissues, IgE-mediated responses are triggered.

Front 52

IgE attaches to ____ within walls of intestine, respiratory tract and skin. ..

Back 52

mast cells

Front 53

What part of IgE binds to mast cell?!

Back 53

Fc region of the antibody attaches to the mast cell

Front 54

Mast cell is part of what immune system?

Back 54

innate

Front 55

Peyer's patches would example of ?

Back 55

Inductive Sites

Front 56

exception to the rule that antibody does not get into cells

Back 56

* B/c IgA is transported through enterocytes, it can act inside these cells
* can bind viral proteins inside these cells and interrupt viral replication.
* example of antibody acting in an intracellular location.

Front 57

Rapid degranulation of mast cells with release of ____ into the tissues leading to ______(3)?

Back 57

Rapid degranulation of mast cells with release of into the tissues leading to:
inflammation, increased vascular permeability, fluid leakage between enterocytes and thus fluid entering the lumen.
~ goal if for parasite to disengage and be flushed out.

Front 58

Antibody dependent cell cytotoxicity (ADCC)
Killer cells that have Fc receptors (monocytes, eosinophils, neutrophils, NK cells) to bind Ab...what class Ab?

Back 58

Mainly IgG, also IgA

Front 59

What is part of Ab that determines its biological class?

What determines specificity?

Back 59

Fc (Fc region of IgA diff. from Fc region of IgG)


Fab

Front 60

Which part of Ab known as constant region?

What part of Ab determines class of Ab (e.g. IgG, IgE)?

Back 60

Fc

Fc

Front 61

Example of protective immunity without sterile immunity (without completely removing antigen)?

Back 61

HIV, Ag bound up but not completely removed

Front 62

Can compliment proteins bind Fc region of Ab?

Back 62

Yes (what does this is trigger)

Front 63

What is cells present in germinal center of Peyer's patches?

Back 63

B cells

Front 64

Which Ab present in highest conc. in colostrum?
Does it contain other antibodies?

Back 64

IgG (to lesser extend IgA, IgE present)

Front 65

What are the two routes of B-cell activation by antigen?

Back 65

T-dependent activation
T-independent activation

Front 66

Are T-dependent antigen usually big or small?

Why are they T dependent?

Back 66

small, soluble antigen

Require T cell to fully activate B cell

Front 67

Type of antibody B cells makes depends on types of cytokines it gets from T helper cells:

Which T cell directs B cell towards more cell mediated response?

Back 67

Th1 cell , get Ab to help mostly with cell mediated response, e.g. involve mostly opsonization, etc

Front 68

What Ab made by T independent antigen?

What type immune response?
What absent?

Back 68

IgM only, short lived

only primary immune response, no secondary (or memory) response, NO class switching

Front 69

What type of hypersensitivity reactions does IgE mediate?

Back 69

Type I hypersensitivity reactions

Front 70

If class switching occurs, what changes about antibodies B cell will make?
What drives class switching?

Back 70

Fc region

cytokines and repetitive

Front 71

Th1 cytokines (IFN-gamma, IL-2) will primarily cause which classes of antibody to be made?

Back 71

IgG
IgM

Front 72

Th2 cytokines (IL-4, IL-5, IL-6) will primarily cause which classes of antibody to be made?

Back 72

IgE
IgA

Front 73

Titer measures ?

Back 73

total Ab in blood

Front 74

Lag phase in primary response? Why slow?

Back 74

primary response slow, hasn't seen Ag before, B cell has to proliferate and differentiate

Front 75

phase characterized by rapid increase in production of Ab, because plasma cells have proliferated

Back 75

Log phase

Front 76

What changes in secondary immune response?

Back 76

lag phase shorter
log phase higher, longer

Front 77

Antibody secretion into lumen occurring in the villi is an example of what kind of site?

Back 77

Effector site

Front 78

What receptor does dimeric IgA bind to on the basal surface of the enterocytes?

Back 78

Poly-Ig receptor

Front 79

What part of the Poly-Ig receptor chain is cleaved off and still attached to the IgA when it enters the lumen? What is this IgA called?

Back 79

Secretory piece
Secretory IgA

Front 80

What antibody mediates immune elimination?

Back 80

IgE

Front 81

Which antibody is 65-90% of total antibody content in most major domestic animals?

Back 81

IgG

Front 82

In pigs and horses what is the dominate antibody in milk?

Back 82

IgA

Front 83

When is the optimal time for absorption of antibodies from colostrum?

Back 83

First 6 hours

Front 84

What are some reasons of failure of passive transfer of antibodies in newborns?

Back 84

Production failure
Ingestion failure
Absorption failure

Front 85

What are some ways that antibody in the serum of the neonate can be evaluated?

Back 85

Salt precipitation or Turbidity tests
Measure total serum protein
ELISA
Radial immunodiffusion

Front 86

How does radial immunodiffusion work?

Back 86

Precipitation ring (serum immunoglobulin reacts with anti-equine immunoglobulin)

Front 87

How long should treatment of failure of passive transfer in the neonate be treated?

Back 87

3 weeks

Front 88

What is the earliest age to vaccinate a puppy or kitten with reasonable expectation of a response?

Back 88

Between 6 and 9 weeks

Front 89

When should you vaccinate calves and foals?

Back 89

Before 6 months (about 4 months0
Re-vaccinate at 6 months or after weaning

Front 90

What Ab most numerous in ruminant milk?

Back 90

1. IgG!!!! = ruminant milk
2. IgA
3. IgE

Front 91

What Ab dominant in non-ruminant milk?

Back 91

1. IgA = non-ruminant milk!!
2. IgG
3. IgE

Front 92

How does neonate internalize IgG present in colostrum?

Back 92

* Maternal IgG binds to Fc Receptor (FcRn) on intestinal epithelial cells of newborn
* Internalized by pinocytosis
* FYI enters lacteals (lymphatic cap.) and intestinal capillaries

Front 93

Why can't neonate take up IgG after 24 hours?

Back 93

After 24 hours a new layer of enterocytes form that prevent absorption because they lack FcRn

Front 94

FIP causes what type of hypersensitivity?

Back 94

Type III

Front 95

Which types of hypersensitivities are mediated by antibody?

Back 95

Type I, II, III

Front 96

Which types of hypersensitivities are mediated by T-cells?

Back 96

Type IV

Front 97

What is a genetically determined predisposition to develop clinical (type-1) allergies?

Back 97

Atopy

Front 98

What is an immediate (type1) hypersensitivity reaction?

Back 98

Allergy

Front 99

What type of allergic reaction is caused by contact with antigen against which the host has pre-existing IgE antibody for?

Back 99

Type I hypersensitivity

Front 100

What are some products released by mast cell granules in type I hypersensitivity reactions?

Back 100

Histamine
Heparin

Front 101

What are the two distinct inflammatory reactions that may occur in type I hypersensitivity reactions?

Back 101

Early phase
Late phase

Front 102

What phase of (type I) inflammatory reactions occur within 10-20 mins of repeat exposure, mediated by histamine and heparin, and sometimes called the "wheel and flare" (on skin!) phase?

Back 102

Early phase

~inhibits clotting allergist does instigates early phase of type I H.S.

Front 103

What phase of inflammatory reaction peaks at 6-12 hours, associated with redness, edema, mucus production and pruritis, and is mediated by chemotactic factors from mast cells?

Back 103

LATE PHASE: this is much more SEVERE swelling that occurs later
e.g. after Walter ate nuts, severe smooth muscle contraction in respiratory tissue
e.g. Asthma attacks

Front 104

What type of hypersensitivity reaction is asthma?

Back 104

Type I hypersensitivity

Front 105

What is the meaning of a "localized" type I reaction?

Back 105

Localized to one organ system

Front 106

Type I hypersensitivity is mediated by what antibody?

Key cell involved?

Back 106

IgE

Mast cell
Also basophil, eosinophils

Front 107

Which animals mainly show liver signs in anaphylactic shock?

Back 107

Dog

Front 108

What is usually the cause of an allergic reaction when given vaccines?

Back 108

Aluminum adjuvants
(acts as hapten?)

Front 109

In Type I hypersensitivity, ___ trigger B cells to make IgE which is inappropriate response for these condition.

Back 109

In Type I hypersensitivity, TH2 cells trigger B cells to make IgE which is inappropriate response.

Front 110

What is a type of skin rash consisting of red, edema, plaque-like eruptions which are often pruritic (itchy)?

Back 110

Urticaria (hives), route of entry does not always indicate system involved in the response

Front 111

What are some diagnostic tests used for Type-I allergies?

Back 111

Measure total IgE in serum
Measure patient IgE specific to suspected allergen
Intradermal skin test

Front 112

What are some treatments of allergic reactions?

Back 112

Inhibit mast degranulation and effects
Inhibit histamines
Corticosteroids
Anti-IgE antibody to neutralize the IgE
Hyposensitization

Front 113

What type of hypersensitivity response is mediated by IgG or IgM?

Back 113

Type II Hypersensitivity

Front 114

Are Type II hypersensitivity reactions cytolytic?

Back 114

Yes

Front 115

What type of hypersensitivity reaction may cause agglutination or hemolysis or stimulate opsonization and phagocytosis of the cells?

Back 115

Type II hypersensitivity

Front 116

What are some examples of type II hypersensitivity reactions?

Back 116

Transfusion reactions
Hemolytic disease of Newborn (neonatal isoerythrolysis)
Immune-mediated cytopenias

Front 117

Are Immune-mediated cytopenias (and Type II HS reactions) a product of autoimmune OR non-autoimmune problem?

Back 117

Immune-mediated cytopenias can be caused by either

Hemolytic disease of Newborn (neonatal isoerythrolysis) is not autoimmune, b/c it's mother's Ab that is causing the problem.

Front 118

What type of hypersensitivity reaction may cause agglutination or hemolysis or stimulate opsonization and phagocytosis of the cells?

Back 118

Type II hypersensitivity

Front 119

If IMMUNE-COMPLEXES of type III hypersensitivity rxn form in TISSUES, what kind of type is it?

Back 119

Local Type-III

Front 120

What are the two types of type II hypersensitivity reactions?

Back 120

Primary type II HS reaction
Secondary type II HS reaction

Front 121

What kind of type II HS reaction is an AUTOIMMUNE disease, where animal makes Ab to surface antigens of RBCs, platelets, or other cells?

Back 121

Primary type II HS reaction

Front 122

What type of type II reaction is when Ab are made to DRUG treatment or an infectious agent?

Back 122

Secondary

Front 123

What is a diagnostic test for an immune-mediated hemolytic anemia?

What would positive Coombs look like?

Back 123

Coombs Test

tests for Ab bound on surface of RBC
- if Ab coating RBC, have a hemolytic situation
- if positive, will see agglutination

Front 124

If an immune-mediated cytopenias (low RBC) is primary how would you treat it?

Back 124

Immunosuppressive drugs

Front 125

If an immune-mediated cytopenias (low RBC) is secondary how would you treat it?

Back 125

Treat for underlying condition

Front 126

What is the cause of a type III hypersensitivity reaction?

Back 126

Formation of immune COMPLEXES b/t antibody (IgG or IgM) and SOLUBLE antigen

Front 127

Which antibody is usually involved in type III hypersensitivity reactions?

Back 127

IgG

Front 128

If the complexes of a type III hypersensitivity reaction form in the tissues what kind of type is it?

Back 128

Local Type-III

Front 129

If the complexes of the a type III hypersensitivity reaction form in the circulation what type is it?

Back 129

Generalized Type-III

= Ab-Ag complex in blood vessel !

Front 130

What are the three mechanisms of Type-III hypersensitivity reactions?

Back 130

Immune complex formation
Immune complex deposition
Immune complex-mediated inflammation

Front 131

What are some examples of Localized type-III reactions?

Back 131

Arthus reaction
Blue eye
Heaves in horses

~localized occurs in TISSUE

Front 132

What are some examples of generalized type-III reactions?*

Back 132

Serum sickness
Glomerulonephritis
Streptococcus equi

note: generalized type III are those that occur in circulation, and for whatever reason complexes frequently accumulate in vessels of kidney and joints

Front 133

How do you treat immune complex conditions?

Back 133

* treat underlying condition (pathogen)
* suppress immune system (glucocorticoids & cyclophosphamide)

Front 134

What is a reaction to IV-injected proteins (usually in antiserum) derived from another species e.g. horse serum?

What type of hypersensitivity is this?

Back 134

Serum sickness - get major Ab-Ag complexes forming in vessels

* this is generalized type III h.s. rxn

Front 135

What do the lesions in serum sickness coincide with?

Back 135

formation of large amounts of immune complexes in circulation

Front 136

What is most of glomerulonephritis in our domestic animal species due to?

Back 136

Immune complex disease

Front 137

What is a hemorrhagic area in the skin?

Back 137

Purpura

Front 138

What is a purpura hemorrhagica due to reduction in circulating blood platelets?

Back 138

Thrombocytopenic purpura

Front 139

What type of purpura is the the purpura hemorrhagica associated with Strep equi?

Back 139

Non-thrombocytopenic purpura

Front 140

What are the general components of any Type-IV hypersensitivity?

Back 140

Antigen sensitized Th1 CD4 lymphocytes and CD8 lymphocytes
Th1 cytokines
Activated macrophages
Response peaks at 72 hours

Front 141

What type of antigens are associated with Delayed-type (type IV) hypersensitivity?

Back 141

Insect venom (proteins)
Mycobacterial proteins

Front 142

What type of antigens are associated with Contact-hypersensitivity (type IV)?

Back 142

Haptens
Pentadecacatechol (poison ivy)
Small metal ions (nickel and chromate)

Front 143

How does the new in vitro TB test work?

Back 143

Based on the ability of mycobacterium tuberculosis antigens to stimulate host sensitized lymphocyte production of IFN-γ

If memory CD4 Th1 present are sensitive to Tb Ag, will proliferate and produce INF-γ which test will detect !!!

Front 144

What kind of type IV hypersensitivity reaction involves haptens binding to skin proteins?

Back 144

Allergic contact dermatitis

Front 145

How should allergic contact dermatitis be treated?

Back 145

Avoid contact with chemical or substance
Anti-inflammatory drugs such as Glucocorticoids
Antibiotics if secondary infection

Front 146

What is the mechanism behind HOST vs graft rejection?

Back 146

Due to reaction against MHC molecules expressed by the tissue graft

Front 147

What is the mechanism behind GRAFT vs host rejection?

Back 147

Foreign lymphocytes in the transplanted bone marrow destroy cells and tissues of the recipient

Front 148

Why may a graft from a male into a female be rejected?

Back 148

HY antigen expressed by male Y chromosome (observed in skin grafts)

Front 149

Ag like pollen, ragweed instigating hypersensitivity is example of what type?

Back 149

Type I w/ IgE

Front 150

Type of Ag that might trigger type 2 HS rxn?

Back 150

Ag on surface of RBC's

Front 151

ADCC is part of what type HS?

Back 151

Type II HS

Front 152

Heparin (chemical mediator causing type 1 hypersensitivity) causes what?

Back 152

inhibition of clotting

Front 153

Histamine causes what?
(aside from inflammation)

Back 153

- vasodilation
- smooth muscle contraction

Front 154

Is bee sting type 1 hypersensitibity?

Back 154

No, that's just irritant

Front 155

hapten

what type H.S. involved in?

Back 155

too small to cause immune response alone, so binds to larger protein (e.g. albumin) or cell and triggers immune response that way
> can cause type 2 or 4 hs.rxn

Front 156

What is Arthus Reaction?
(give example and describe what happens)

Back 156

Arthus reaction e.g. tetanus toxoid vaccine causes Type III hypers.
* If give subQ inj. into animal that already has Ab to antigen, can form complexes (usually IgG), then acute inflammation will develop, CC (Ab-dependent pathway aka specific/classical)

Front 157

Blue Eye in dogs

Back 157

causes localized type III h.s. rxn

*some dogs infected with canine adenovirus type 1 or vaccinated with modified live CAV type 1 vaccine.
Lesion: anterior uveitis leading to corneal edema and opacity.
* Virus-antibody complexes, neutrophils present in lesion.