Most recognized mediator of type 1 hypersensitivity reactions.
Type of graft if donor and recipient are the same
A catastrophic, systemic life threatening IgE mediated hypersensitivity reaction.
Localized immune reaction seen with discrete tissue necrosis, usually in skin.
Mast cells, Basophilks and these are essential to the development of type 1 hypersensitivity reactions.
In this disease, autoantibodies bind and activate thyroid stimulating hormone
These stem cells can be harvested from bone marrow or peripheral blood
This type 1V hypersensitivity reaction is most common with this clinical material.
Typical blood vessel reaction with degranulation and release of mediators.
Agent responsible for farmer's lung
Absence of normal immune response to a certain antigen
Type of graft if donor and recipient are identical twins.
Skin test to determine if an individual has been exposed to TB.
Disease is considered autoimmune, and results from wheat consumption
Autoimmune disorder, body cannot distinguish between self and ________
Molecular process, foreign antigen is similar to own autoantigen, triggering an immune response.
Down
Syndrome of thymic hypoplasia
HLA molecules recognized as foreign on allografts.
Autoimmune arthritis
Antibody dependent cell cytotoxicity has been implicated in the development of _________ vulgaris.
This allergic condition is a common hypersensitivity disorder of the upper respiratory tract.
Process by which organism acts against its own tissue
Chediak-Higashi syndrome is considered a primary disorder of____________
Cell name that directly becomes antibody
Type 111 reactions are responsible for this condition, seen in SLE and acute glomerulonephritis
In type 1 hypersensitivity reaction, antigens are also referred to as these.
Type of resulting edema that is life threatening by complete airway obstruction
Class 1 MHC molecules present these type of antigens, synthesized inside the cell.
Local hypersensitivity reaction where offending allergen is confined to a particular site.
This sickness results from formation of insoluble antigen-antibody complexes in antigen excess
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