immunologic disease processing

hypersensitivity

an exaggerated or inappropriate ADAPTIVE immune response to NON-SELF antigens

autoimmunity

an ADAPTIVE immune response to SELF antigens

immunodeficiency

a decrease in function of the immune system

what type of immunodeficiency is linked with genetic cause?

primary immunodeficiency

what type of immunodeficiency is linked with a cause besides genetics?

secondary immunodeficiency

can immune deficiencies involve either the innate immune system and/or the adaptive immune system?

yes

what is the only type immune system involved with hypersensitivities and autoimmunities? why?

adaptive immune system since it involves and abnormal response to an antigen

what cells are involved with acute inflammation?

neutrophils first then macrophages

what cells are involved with chronic inflammation?

macrophages, lymphocytes, plasma cells, and eosinophils

what type of cell is producing an intense immune response to wet form of FIP?

Th-2 cells lead to intense antibody-antigen complexes to form in the blood and deposit on endothelium

what is the first step in any hypersensitivity?

need a primary response to the antigen = sensitization period (7-10 days)

no clinical signs show up until...

1. antigen shows up again

2. antigen persists through out the sensitization period

what types of hypersensitivities are mediated by antibodies?

type 1, 2, and 3

what types of hypersensitivities are mediated by a cell-mediated response to antigen?

type 4

what cells are involved in type 1 hypersensitivities?

mast cells, Th-2 cells, IgE, and histamine release

what do Th-2 cells promote in type 1 hypersensitivities?

promote B cells to make IgE

what is the timeline for type 1 hypersensitivity after sensitization?

within 30 minutes

what is the timeline for type 2 hypersensitivity after sensitization?

5-8 hours

what is the timeline for type 3 hypersensitivity after sensitization?

2-8 hours

what is the timeline for type 4 hypersensitivity after sensitization?

24-72 hours

type 2 hypersensitivity

host cell altered or destroyed

type 3 hypersensitivity

soluble antigen-antibody complexes deposit in blood vessels of tissues and cause inflammation

what is the antibody-antigen complex in type 3 hypersensitivities?

IgG binds antigen in solution

what cells are involved in type 4 hypersensitivities?

Th-1 cells, Th-1 cytokines, macrophages, and CTLs

what response is associated with type 4 hypersensitivities?

DTH

what type of hypersensitivity is associated with anaphylactic shock?

type 1

what reactions are associated with type 1 hypersensitivities?

immediate allergic reactions

what is the mechanism of type 1 hypersensitivities?

1. Th-2 cells release too much IgE due to cytokine activation

2. IgE binds to Fc part of mast cells

3. when allergen shows up again the IgE on mast cell leads mast cell to degranulate and release chemical mediators

histamine

the main mediator in type-1 hypersensitivities

if you had a mast cell that already had IgE binded, what would this indicate?

sensitization has already occurred in mast cell since it already has a product from antigen exposure

why does degranulation occur in mast cells?

in second exposure to antigen, the allergen will bind to Fab region of mast cell

what does the severity and location of type 1 hypersensitivities depend on?

1. degree of sensitization

2. amount of antigen involved

3. route of encounter with antigen

type-1 reactions include (physiological effects)

1. smooth muscle contraction

2. vasodilation

3. mucus production

what is the result of anaphylactic shock?

1. smooth muscle contraction ( bronchial restriction)

2. vasodilation (drop in blood pressure)

3. increase in vascular permeability (edema)

4. mucus production

what immunoglobulin mediates type-2 hypersensitivities?

mainly IgG but can also be IgM

what happens during a type-2 hypersensitivity?

pre-existing specific antibody binds to antigens on the surface of hosts cells via Fab region leading to destruction or alteration of host cells

what are examples of type-2 hypersensitivities?

1. immune-mediated hemolytic anemia

2. grave's disease

immune-mediated hemolytic anemia

IgG on RBC leads to their destruction

what are potential causes of immune-mediated hemolytic anemia?

1. autoimmune

2. secondary to a drug (penicillin)

3. infection

what causes vasculititis in type-3 hypersensitivities?

immune complexes that were not removed by phagocytic cells deposit on inside of blood vessel along endothelium leading to inflammation of blood vessel

what are signs related to vasculitis?

1. rash (skin)

2. protein in urine

3. joint pain

what immunoglobulin is associated with type-3 hypersensitivities?

mainly IgG, sometimes IgM

Type 4 hypersensitivity

1. antigen activated Th-1 cells produce IGN-g and IL-2

2. IFN-g activates macrophages

3. lead to damage and inflammation

what are antigens often in typer 4 hypersensitivities?

haptens

what are examples of type-4 hypersensitivities?

1. poison ivy

2. topical drugs

3. immune mediated contact dermatitis

skin reaction to topical penicillin would be an example of what type of hypersensitivity?

type 4

a blood transfusion reaction would be an example of what type of hypersensitivity?

type 2

an autoimmune disease due to antibody directed against a host cell receptor molecule would be an example of what type of hypersensitivity?

type 2

Pemphigus foliaceous in dogs is associated with which type of autoimmunity?

primary

molecular mimicry due to infection would be an example of what type of autoimmunity?

secondary

immunodeficiencies

decreased ability of the immune system

FIV infection causes infection and destruction of CD4-T lymphocytes. What type of immunodeficiency is this and what part of the immune system?

secondary immunodeficiency of the adaptive immune system

Canine leukocyte adhesion deficiency causes neutrophils to be unable to get out of circulation. What type of immunodeficiency id this and what part of the immune system?

primary immunodeficiency of the innate immune system

what is the difference between primary and secondary immunodeficiencies?

the cause