hypersensitivity

Question 1

what is hypersensitivity

Answer 1

Hypersensitivity reactions occur when the immune system mounts an excessive response to a stimulus. This includes an excessive response to an infectious agent or to self-antigen resulting in autoimmune disease.

Question 2

what 4 types hypersensitivity

Answer 2

Type I- Allergic reactions
Type II- AntiBbody-mediated cytotoxicity
Type III- Immune complex deposition
Type IV- Delayed type (cellular)

Question 3

type I hypersensitivity

Answer 3

• Type I hypersensitivity results in rapid clinical manifestations, and underlies many disorders widely recognised as ‘allergies’ such as hay fever and asthma.
•In individuals predisposed to Type I hypersensitivity, antigen exposure leads to IgE production.
•IgE binds Fc receptors on mast cells, packed with granules containing histamine and other preformed mediators.
• IgE cross-linking by allergen (re-exposure) causes degranulation of mast cells and rapid release of mediators

Question 4

mediators release in hypersensitivity type I

Answer 4

histamine, serotonin, leukotrienes and proteases.

Question 5

clinical manifestations of type I hypersensitivity

Answer 5

rhinitis, asthma, and, in severe cases, anaphylaxis

Question 6

duration type I hypersensitivity

Answer 6

Type I hypersensitivity reactions are rapid, occurring within minutes after challenge (reexposure to antigen).

Question 7

allergic reaction also called ?

Answer 7

immediate hypersensitivity

Question 8

type II hypersensitivity

Answer 8

Type II hypersensitivity involves antibody-mediated destruction of the cells.
• Usually IgG is involved and complement activation follows.
•Antibody can also mediate killing by antibody-dependent cell- mediated cytotoxicity (ADCC), wherein the cytotoxic cells with Fc receptors bind to Fc region of antibodies on target cell and promote killing of the cells.
• Antibody bound to foreign cells may also serve as opsonin and facilitate phagocytosis.

Question 9

3 different antibody mediated responses are involved in type II hypersensitivity reactions.

Answer 9

Usually 3 different antibody mediated responses are involved in type II hypersensitivity reactions. The targeted cell is either damaged or destroyed through a variety of mechanisms associated with:

• complement-mediated reactions
• antibody-dependent cell- mediated cytotoxicity
• antibody-mediated cellular dysfunction

Question 10

Type II Hypersensitivity - Examples

Answer 10

•Goodpasture’s disease - antibodies to glomerular basement membrane bind to basement membrane in kidney and lung. Bound antibody cannot be removed by phagocytosis and intense inflammation results.
• Myasthenia gravis - antibodies bind to acetylcholine receptors at the motor end plate, reducing the ability of nerve impulses to activate muscles.
• Graves’ disease - antibodies bind to the TSH receptor and induce thyroxine production leading to hyperthyroidism.
• Other examples include: • Transfusion reactions
• Drug-induced reactions
• Rhesus incompatibility reactions

Question 11

Type III Hypersensitivity

Answer 11

Type III hypersensitivity results from formation or deposition of immune complexes (ICs) in tissues. ICs may be formed in the blood and trapped in tissues.
•When antigen binds antibody, complement is activated and neutrophils and other inflammatory cells are attracted. Phagocytic cells ingest the immune complexes.
• However, when the capacity to clear complexes is exceeded, immune complexes of a certain size can inappropriately deposit in the tissues and trigger a variety of systemic pathogenic events known as type III hypersensitivity reactions.

Question 12

where type III hypersensitivity reactions occur

Answer 12

These type III hypersensitivity reactions can be systemic or localized and can be associated with immune complex deposition in the kidneys, skin, joints, choroid plexus, and ciliary artery of the eye.

Question 13

generation of immune complex in type III hypersensitivity stimulated by ?

Answer 13

•The generation of immune complexes can be stimulated by exogenous antigens such as bacteria and viruses or, as in the case of the Arthus reaction by intradermal or intrapulmonary exposure to large amounts of foreign protein.
• Alternatively, endogenous antigens, such as DNA, can serve as a target for autoantibodies as seen in systemic lupus erythematosus (SLE).

Question 14

Type III Hypersensitivity - Examples
• Systemic immune complex diseases

Answer 14

Systemic immune complex diseases
• Serum sickness
• Rheumatic fever
• Rheumatoid arthri

Question 15

Type III Hypersensitivity - Examples
Localized immune complex diseases

Answer 15

Localized immune complex diseases
• Arthus reaction – Farmer’s lung
• Other occupational diseases -pigeon breeder’s disease, thatched roof worker’s lung

Question 16

Type IV Hypersensitivity also known as?

Answer 16

delayed-type hypersensitivity reactions (DTH).

Question 17

Type IV Hypersensitivity

Answer 17

• Type IV hypersensitivity is due to activation of cellular immunity and the onset of clinical manifestations is typically delayed by 48–72 hours.
• Antigen is taken up by antigen presenting cells (APCs), which then migrate to regional lymph nodes. Following antigen processing, APCs present antigen to responsive T cells, which proliferate and mature.
• Antigen specific Th1 cells then migrate to the periphery and when they encounter antigen are further stimulated. They secrete IFN which activates macrophages, and both T cells and macrophage
• DTH reactions are, therefore, cell-mediated immune responses. Depending on the antigen involved, they mediate beneficial (resistance to viruses, bacteria, fungi, and tumors) or harmful (allergic dermatitis, autoimmunity) aspects of immune function.

Question 18

Type IV Hypersensitivity - Examples

Answer 18

• Tuberculin reaction / PPD / Mantoux test • Contact dermatitis
– exposure to poison ivy plant
• Allograft rejection
• Autoimmune diseases – Multiple sclerosis