Immune Attack On Tissues: Hypersensitivity, Allergy And Transplant Rejection Flashcards Preview

CLS 2 > Immune Attack On Tissues: Hypersensitivity, Allergy And Transplant Rejection > Flashcards

Flashcards in Immune Attack On Tissues: Hypersensitivity, Allergy And Transplant Rejection Deck (21)

Immunity, allergy and autoimmunity: self or foreign

Material recognised->material damaged-> result
Foreign-> foreign-> immunity
Foreign-> self-> allergy
Self-> self-> autoimmunity


Type 1 hypersensitivity definition

Atopic allergy
Antibody mediated
Damage to self tissue triggered bŷ an adaptive immune response to non infectious agents


Type 1 hypersensitivy mechanism, immediate

Often harmless antigen reacts with specific IgE antibodies located on mast cells and basophils.
-> rapid release of preformed chemicals from mast cell
-> histamine-> vasoactive and inflammatory
->Leukotrienes and prostaglandins-> vasodilation, smooth muscle spasm, vasopermeability, excessive epithelial secretion


Type 1 hypersensitivy mechanism, late

Chronic response
Antigen is presented to Th2 cells
-> produce IL-4
-> stimulates B cells to produce IgE ->IgE binds mast cells->IgE-mast cell complex -> if exposed to antigen again-> reaction
Also produce IL-5-> stimulates eosinophils
Chronic tissue damage as a result of cytokines and eosinophil products



Common allergens-> drugs, serums, venoms, peanuts
Route of entry-> intravenous or oral absorption
Responses-> edema, increased vasuclar permeability, tracheal occlusion, circulatory collapse, death
Acute widespread effects due to antigen reaching the blood stream


Acute urticaria

Wheal and flare
Allergens-> insect bites! allergy testing
Route of entry-> subcutaneous
Response-> local increase in blood flow and vascular permeability


Allergic rhinitis

Allergens-> pollens, dust mite faeces
Route of entry-> inhalation
Responses-> edema of nasal mucosa, irritation of nasal mucosa



Allergens-> danders (cat), pollens, dust mite faeces
Route of entry-> inhalation
Responses-> bronchial constriction! increased mucous production! airway inflammation
Inflammatory mediators increase mucous production-> acute response
Cytokines and eosinophils-> chronic response


Food allergy

Route of entry-> oral
Response-> d and v, pruritis, urticaria (hives), anaphylaxis


Skin prick test

Tests for sensitivity to specific allergens by intra dermal exposure
-> induces a wheel and flare reaction if allergic
Immediate-> redness and inflammation 15-60mins
Immediate + late-> redness and inflammation, appearance of IgE and T cells at 4-12 hours, disappear after 48
Delayed-> no redness till 12-48 hrs after appearance of Th1 cells
Eczematous test-> redness at 15-60mins, IgE and Th2 at 12-48 hrs-> broken skin


Type II hypersensitivity definition

Circulating antibodies attaching to specific body antigens leading to death of the cells and tissues bearing the specific antigen


Type II hypersensitivity mechanism

IgG, IgA or IgM antibodies bind to cell surface antigens
Results in antibody coated cells
Induces damage either by:
Lysis via activation of the complement system, cells can't be phagocytosed so neutrophils secrete lysosomes
Or by killer cells directed against antibody covered cells
May also be phagocytosed by macrophages
Requires at least two IgG bound to target.


Examples of type II hypersensitivity

-Immune haemolytic anaemia:
Allergic haemolytic anaemia
Autoimmune haemolytic anaemia
Blood transfusion reactions
Haemolytic disease of new born
Drug induced-> IgG specific for drugs that bind to the surface of RBC allergy.
-autoimmune thrombocytopenia
-pemphigold (skin)
-goodpastures disease
-myasthenia gravis
-Graves' disease


Type III hypersensitivity, definition

A normal response becomes excessive
Deposition of soluble circulating antigen-antibody complexes in vessel walls or other tissues
Characterised by vasculitis-> firbinoid necrosis of small blood vessel walls
Low blood complement
Small complexes excredted


Type III hypersensitivity, mechanism

Several soluble antigens and antibodies cross link to form a lattice-> immune complex
Immune complex becomes lodged in tissues when too much is produced and can't be removed fast enough
-> activate complement-> attract neutrophils
Neutrophils and factors attracted by platelets initiate the damage-> tissue inflammation and necrosis


Type III hypersensitivity examples

Allergic alveolitis
Production of antibodies in response to inhaled fungal spores
Immune complexes form in alveoli walls leading inflammation and fibrosis
Results in breathlessness due to poor gas exchange


Type IV hypersensitivity definition

Cell mediated, no antibodies involved
Caused by sensitised T lymphocytes


Type IV hypersensitivity, mechanism

Sensitised T lymphocytes contact with a specific antigen
-> release cytokines
-> IL-2-> activates Tc cells
-> IFN-Y activates macrophages-> granuloma formation
Large numbers of lymphocytes and macrophages


Type 3 hypersensitivity, examples

Reactions stimulated by Microorganisms-> TB and leprosy, also some fungi-> candidiasis
Contact dermatitis-> react with carrier protein in the skin
Acute graft rejection
Adrenal it's
Type diabetes


Transplant rejection, definition

Transplanted tissue destroyed by the immune system
Cell mediated hypersensitivity
Blood group and HLA antigens must match


Acute graft rejection, mechanism

Major stimulus is differences between HLA proteins of donor and recipient that are recognised by T cells of the recipient
T cells react against HLA particularly type 2
Graft becomes infiltrated with lymphocytes-> t cells and macrophages
Recognition can be->
Direct-> by recognition of HLA proteins on antigen presenting cells of donor origin in lymph
Indirect-> recognition of peptides derived from donor proteins presented by recipients APCs

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