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Immunology - Hypersensitivity Reactions (dropped image link…
Immunology - Hypersensitivity Reactions
Hypersensitivity Reactions are
1234 ABCD ACID
A A = allergic and Atopic
C B = cytotoxic and antiBody
I C = immune complexes (IgG and IgM) --> SLE
D D = Delayed (contact Dermititis = poision ivy)
*Type 1 Hypersensitivity Reaction
immediate IgE allergic reaction
mostly IgE mediated
Clinical Cases
Clinical Case
Clinical Case
Notes
:
note that
Allergic Reaction example
Notes
:
note that in an allergic reaction, the first exposure ever to the antigen has a class switch from IgM to IgE antibodies that bind to the specific antigen
these IgE are now ready in B cells to be released if the antigen = allergen ever enters again
second exposure --> these IgE antibodies bind to basophils and mast cells = granulocytes
--> cause them to release granules, cytokines, and interleukins
--> histamine, leukotrienes, proteases, prostaglandins, etc.
Clinical Case
Allergic Reaction example 2
Notes
:
note that the IgE that are produced for people who have allergies, these are not just free floating antibodies in the tissues or blood,
they are mostly
IgE antibodies that are surface bound to granulocytes like basophils and mast cells
once the antgien or allergen enters the tissue it binds to IgE on these granulocytes and they release histamine, etc.
Clinical Case
3 phases of Type 1 rxns
1 =
Prephase
= sensitization tot he antigen
--> makes IgE antibodies that attach to mast cells and antibodies
2 =
Immediate
inflammation phase = release of preformed IgE and tryptase
--> tryptase levels used for diagnosis
3 =
Delayed
inflammation phase = infiltration and inflammation from the cytokines left over from the early phase of type 1 rxn
--> proteases cause most of delayed phase
2 = Immediate inflammation phase
2 =
Immediate
inflammation phase = release of preformed IgE and tryptase
--> tryptase levels used for diagnosis
Binding of the antigen to IgE on
antigen IgE binding
--> on high affinity FcER IgE recetors are specific binders to the Fc portions of antibodies
Aggregation of the high affinity FcER IgE recetors
agregation of multiple receptors to one antigen is what causes the release of granules from the mast cells and basophils
this makes sense since the level of reaction response depends on the sensitization to the antigen and how much IgE you have made
thus more exposure
--> more IgE bound to high affinity receptors
--> more high affinity IgE receptors can aggregate and release more granules
1 more item...
3 = Delayed inflammation phase
3 =
Delayed
inflammation phase = infiltration and inflammation from the cytokines left over from the early phase of type 1 rxn
--> proteases cause most of delayed phase
Prephase
= sensitization to the antigen
makes IgE antibodies that attach to mast cells and antibodies
2 =
Immediate
inflammation phase = release of preformed histamine and tryptase
--> tryptase levels used for diagnosis
3 =
Delayed
inflammation phase = infiltration and inflammation from the cytokines left over from the early phase of type 1 rxn
--> proteases cause most of delayed phase
depends on also the prephase granules that are present inside of mast cells and basophils
*Preformed Granules of mast cells and basophils
depends on also the prephase granules that are present inside of mast cells and basophils
*IgE Fc attachment to mast cells and basophiles
important for prephase of hypersensitivity type 1 rxns
high affinity FcER IgE recetors are specific binders to the Fc portions of antibodies
*Type 2 Hypersensitivity Reaction
Cytotoxic IgM and IgG
*Type 3 Hypersensitivity Reaction
Immune Complex
Henoch-Schonlein Purpura
IgA complexes --> systemic vasculitis
remember the
"HENOCH PAAAPacy"
= pope Henoch-Schonlein German pope fictional
"HENOCH PAAAPacy"
= pope Henoch-Schonlein German pope fictional
PAAAP
= purpura
A
= IgA complexes cause vasculitis systemicall
arthralgia
= from the IgA complexes collecting in joints
Abdominal pain
= again from the IgA
Henoch-Schonlein Purpura case
Notes
:
note that HS purpura present with PAAAP as in this case
Case presentation:
Acute Serum Sickness = ASS Type reaction
FAP symptoms = fever arthralgias, Pruritic rash
1-2 wks post Mabs or Abx or venom
ASS example
Case presentation:
Notes
:
note that ASS = acute serum sickness is a common way people who are allergic to certain medications or venom
--> happens 1 wk - 2wks after being given them
type 3 hypersensitivity reaction
immune complexes of IgM and IgG and also complement cytokine = C3 get depositied in tissues and cause pruritic rashes and fever and
FAP symptoms = fever arthralgias, Pruritic rash
note that because you get these depositions int he issue of the Imune complexes and the C3, you have less c3 total circulating in the blood
*Type 4 Hypersensitivity Reaction
delayed type --> t cells (CD8 mostly) and macrophages
contact dermitidis = poison ivy
reactive skin testing (tuberculin TB skin test)
take 48 -72 hours
*Antigen skin testing (Tuberculin TB)
Type 4 Hypersensitivity Reaction
also candida injection for general CD8 testing
3 key cells respond to the antigen skin test
--> macrophages
--> CD4 T cells
--> CD8 T cells
*Tuberculin skin testing (Tuberculin TB)
Type 4 Hypersensitivity Reaction
also candida injection for general CD8 testing
Clinical Cases
Clinical Case
Clinical Case
Notes
:
note that
*Candida Antigen skin testing
note that virtually all people react to the candida antigen so this is used as a control
only people who would not rect to it are SCID or other immunodeficient people
*Poison ivy Dermatitis
Type 4 Hypersensitivity Reaction
Clinical Cases
Posion Ivy Dermatitis
Notes
:
note that Poison Ivy Dermatitis is a type 4 hypersensitivity reaction
--> think that it usually takes a few days for poison ivy dermatitis to actually appear
Case presentation:
Clinical Case
Clinical Case
Notes
:
note that
*DIRTY USMLE
Cmooth depostion = Good Pasture = 2 words = type 2 reaction
Cmooth depostion = Good Pasture
lump-I bumby-I depostiion = Immune Complex Depostin = ICD = 3 words = TYPE 3 reaction
ICD = PSG = lump-I bumby-I depostiion
*TB test = type 4 DELAYED reaction
classic example of type 4 reaction
since for a TB test you have to wait 48-72 hours for there to be a reaction
this means it is type 4 reaction and Macrophages peak at day 3 after inflammation
--> hence type 4
--> TH1 activating = macrophages and CD8+ cells