Hypersensitivity Autoimmunity Flashcards
Hypersensitivity
- A group of disorders where the normally beneficial components of the immune response act in an exaggerated or inappropriate fashion to environmental antigens which do not normally cause tissue damage.
- The exaggerated response, rather than the antigen itself is responsible for the tissue damage which results (bystander damage).
Atopy
- A genetic tendency to produce IgE to normally innocuous, common environmental allergens
- (40% of population)
Allergy
- A clinical expression of the atopic tendency
- (15-20% of population)
Factors that affect hypersenitivity
- Genetics
- Environment e.g Allergin
- Immune dysregulation
- Internal influences
TYPE I HYPERSENSITIVITY
- This is where the body recognises an environmental antigen as a pathogen and releases IgE and triggers Mast cell responses.
- During sensitisation, the allergen is shown to a T helper cell by an antigen presenting cell. This causes B cells to differentiate to produce IgE against the antigen.
- From then onwards, exposure to the antigen will cause the release of cytokines from Mast cells, resulting in an allergic response.
- Immediate type hypersensitivity
Things involved:
- Allergens/allergy
- IgE
- Th2 cells
- Mast cells
- Granule associated inflammatory mediators
- Newly-made inflammatory mediators
- Atopy► ( genetic tendency to develop allergic diseases e.g asthma)
TYPE II HYPERSENSITIVITY
- In this type, the body’s antibodies bind to the antigens on its own cell surfaces.
- Antibodies are produced in response to the antigens on the cell surfaces e.g. when penicillin binds to blood cells
- IgG and IgM antibodies trigger the complement system causing cell lysis
Things involved:
- Antibodies
- Complement
- Fc receptors
- ADCC (antibody‐dependent cell‐mediated cytotoxicity)
Type III
- This form of hypersensitivity is characterised by the formation of immune complexes (clumps of antibodies that have stuck together)
- A low conc. of antibody coupled with a large conc. of antigen causes small complexes to form
Things involved:
- Anitgen-antibodies formation
- Local arthus
- Systemic serum sickness reactions
Type IV
- The body’s CD4 helper T cells recognise the foreign antigen, and starts to produce cytokines which leads to an inflammatory response.
- Delayed type hypersensitivity
Things involved:
- Haptens (binds to proteins to make antibodies)
- Carrier proteins
- Th1 cells
- Antigen-presenting cells
- Monocytes/macrophage
- Granuloma formation
Explain the pathophysiology of early and late phase reactions ►
o Early Phase Response
- Occurs within minutes
- Preformed mast cell mediators( histamine, heparin, chemotactic factors, tryptase, chymase, eosinophil/neutrophil )
o Late Phase Response
- Newly synthesised mediators (Prostaglandins, leukotrienes)
- Th2 cytokines
- Eosinophil mediators
Define the pathophysiology of immune complex formation in localised and systemic Type III Hypersensitivity?
o Localised
- Causes localised inflammation and can be cleared away by macrophages
o Systemic
- Complexes are deposited in tissues and organs such as the skin, joints kidneys and blood vessels
Define the term autoimmune disease
A large group of clinical disorders characterised by tissue or organ damage mediated by incorrect immune mechanisms targeted at self-antigens.
Illustrate the factors involved in the aetiology of autoimmune disease►
Caused by an interaction of
o Genetic Factors
o Immune Regulatory Factors
o Hormonal Factors
o Environmental Factors
Describe the pathogenic mechanisms involved in autoimmune disease►
o Cell-mediated
o Antibody-mediated
o Antibody + Complement
o Immune Complex-mediated
o Recruitment of innate compunds
List the organ specific autoimmune disease►
- Thyroid
· Hashimoto’s Thyroiditis
· Primary Myxoedema
· Thyrotoxicosis
- Stomach
· Pernicious Anaemia
- Adrenal
· Addison’s Disease
List the non-organ specific autoimmune disease.►
· Dermatomyositis - Skin
· Scleroderma- kidneys
· SLE (Systemic Lupus Erythematosus )- Joints
· Rheumatoid Arthritis
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