Autoimmunity, hypersensitivity and skin Flashcards Preview

Blood, Immunity and Infection > Autoimmunity, hypersensitivity and skin > Flashcards

Flashcards in Autoimmunity, hypersensitivity and skin Deck (20):
1

4 classes of hypersensitivity, based on Gel and Coombs

1: IgE mediated (allergic or anaphylactic)
2: IgG, cytotoxic
3: IgG immune complex mediated
4: T cell (DTH delayed)

2

Where does IgE bind to and what does it cause?
What else can cause this?

FcER's on mast cells, and causes cross linking resulting in mast cell degranulation.

C3a, C5a and some drugs

3

What are the actions of granules released from mast cells

Chemoattractants
Activators: vasodilation, complement, platelets
Spasmogens: SM contraction, mucus secretions

4

Common allergies

Rhinitis: dust mites, pollen, animal dander
Insect stings: proteins in toxin (anaphylaxis can occur)
Food: peanuts, wheat, strawberries, milk proteins (in GALT)
Drugs: penicillin, codeine, morphine

5

Allergies treatment

-Avoidance
-Antihistamines
-Corticosteroids
-Sodium cromoglycate (stabilises mast cells)
-Sympathomimetics: norepinephrine/epinephrine in anaphylaxis
-Desensitisation: gradually increasing dose of allergen to induce IgG reaction

6

How does type 2 hypersensitivity work (antibodies against cell surface)

ADCC due to binding of killer cell to IgG on cell surface
Complement, leading to MAC and C3b leads to
Frustrated phagocytosis (release granules)

7

Type 2 hypersensitivity and haemolytic disease of the newborn- Anti RhD red cell IgG antibodies.
Is an example of _____ ____ autoimmunity

-RhD _ mother with RhD _ fetus
-First birth it is ____, but at birth, some ___ ____ are mixed, and mother makes ___ ____ antibodies IgG (post partum)
-IgG _____ transported into ____, and these ___ ___ antibodies go into ____ circulation and ___ the red cells.

-to prevent at ___ inject some ___ ____ antibodies to lyse babies red cells before immune response

Organ specific
-RhD - mother with RhD + fetus
-First birth it is fine, but at birth, some red cells are mixed, and mother makes anti RhD antibodies IgG (post partum)
-IgG actively transported into placenta, and these anti RhD antibodies go into babies circulation and lyse the red cells.

-to prevent at birth inject some anti-RhD antibodies to lyse babies red cells before immune response

8

Type 3 hypersensitivity

Following ____ infection, when antibodies appear when antigen concentrations are ++, some ____ larger than normal immune ---- are formed.
These large immune complexes can be deposited in ___ ____, cause microthrombi and platelet aggregation. Importantly ____ can be activated as well as ____ binding and degranulation leading to damage, ____.

Following chronic infection, when antibodies appear when antigen concentrations are high, some soluble larger than normal immune complexes are formed.
These large immune complexes can be deposited in blood vessels, cause microthrombi and platelet aggregation. Importantly complement can be activated as well as neutrophil binding and degranulation leading to damage, vasculitis.

9

Mantoux test

Type 4 hypersensitivity
Antigens (TB, candida, mumps) introduced under skin.
CD4 TH cells invade, release cytokines and causes swelling and redness as other cells are recruited.
Used to tests memory

10

Contact sensitivity

Example of type 4.
Exposure, to some things like ___ ____ (nickel) or other being taken up by ____ in the ))) and presented to ____ cells.

Usualy antigens to ___ to invoke response, so have binded to normal ____ in the skin, act as a carrier (____).
When memory cells return, invoke inflammation

Example of type 4.
Exposure, to some things like metal ions (nickel) or other being taken up by APC's in the skin and presented to TH1 cells.

Usualy antigens to small to invoke response, so have binded to normal proteins in the skin, act as a carrier (hapten).
When memory cells return, invoke inflammation

11

Autoimmunity involves what hypersensitivity reaction

2 : organ specific
3: systemic

12

Examples of autoantibodies

-Natural IgM low affinity
-ANA, anti-nuclear antibody: seen in SLE, and elderly
-Anti-thyroid, often low affinity, seen in thyroid disease

Autoantibodies common, disease is rare

13

Mechanisms of tolerance

-Clonal deletion (central): in bine marrow and thymus
-Clonal regulation (peripheral): no co-stimulation, anergy
-Suppression (peripheral): Tregs control self reactive cells
-Ignorance: privileged sites

14

Autoimmunity through molecular mimicry

bacterial antigen similar to self, dependent on HLA phenotype as not everyone presents same peptides

15

Examples of organ specific autoimmunity

** not test

-Goodpastures syndrome: Antibodies against type IV collagen in glomerular basement membrane
-Hashimotos thyroiditis
-Myasthenia gravis: antibodies against Ach receptors
-Idiopathic thrombocytopenic purpura ITP: antibodies against platelets-petechia
-Addisons: antibodies against adrenal cortex, hyperpigmentation
-Type 1 diabetes
-Pernicious anaemia: autoantibodies on IF
-Graves disease: Anti- TSH antibody that stimulates thyroxine, thyrotoxicosis. Low TSH. can cause exopthalmos

16

Systemic autoimmune disease

Soluble antigen and antibodies in optimal conc: precipitation and vessel deposition and type 3
Kidneys: glomerulonephritis, skin-rash, joints, arthritis

17

Two most common systemic autoimmune diseases

SLE and rheumatoid arthritis

18

Genetic predisposition and autoimmune diseases (systemic or no?)

Antigen receptor genes; antigen presentation genes (HLA); complement genes; regulatory genes

19

MHC association, not exam however shows antigen presentation or T cell repertoire problem.

Also gender bias towards females

Ankylosing spondylitis and HLA-B27* progress??
Goodpastures and HLA DR2
Addisons and HLA DR3
RA and HLA DR4

20

Autoimmune treatment

Replacement: IDDM: insulin injections; hashimotos: thyroxine; Addisons: GC and MC. Better for organ specific

Suppresion, systemic: SLE: immunosuppresive, corticosteroids, azathioprine, cyclophophamide
RA; corticosteroids, anti-inflams (NSAIDS), anti-TNF-a, IL-1 and 6, gold,