Immune Response and Hypersensitivity Quiz

What is the term for the inappropriate immune response that can result in significant tissue damage or death?

Which molecules induce a localized inflammatory response to eliminate antigen without extensively damaging the host's tissue?

What do effector molecules act to remove?

What is the primary role of the battery of effector molecules in an immune response?

Which type of hypersensitivity reaction is initiated by antibody-antigen complexes?

In which type of hypersensitivity reaction do the symptoms manifest in days?

Which immune response is associated with delayed-type hypersensitivity?

Which immune response is associated with immediate hypersensitivity?

Which type of hypersensitivity reaction ?

What type of hypersensitivity reaction is induced by antigens known as allergens?

Which portion of IgE binds with Fc receptors on mast cells and basophils?

What is the term for mast cells and basophils coated by IgE?

What causes degranulation of sensitized mast cells and basophils?

What is the term for the hereditary predisposition to development of immediate hypersensitivity reactions to common environmental antigens?

What is the term specifically used for nonparasitic antigens capable of stimulating type I hypersensitive responses in allergic individuals?

What is the lowest of all antibody classes in serum and has a half-life of 2-3 days but once bound to mast cells or basophils, can last for weeks?

Which cells bind IgE and are responsible for the symptoms of immediate hypersensitivity reactions?

Type I hypersensitivity reactions are mediated by nonparasitic antigens known as allergens.

IgE has the lowest half-life of all antibody classes in serum.

The reaginic activity of IgE depends on its ability to bind to a receptor specific for the Fc region of the ε heavy chain.

What initiates IgE-mediated degranulation in mast cells and basophils?

What results in mast cell degranulation following IgE cross-linkage?

Which drug is highlighted for its ability to block the increase of Ca2+ as a treatment for allergies?

What is necessary for the movement of granules to the plasma membrane during mast cell degranulation?

IgE cross-linkage initiates degranulation in mast cells and basophils.

The increase of Ca2+ is not necessary for mast-cell degranulation.

Drugs like disodium cromoglycate (cromolyn sodium) promote Ca++ influx during degranulation as a treatment for allergies.

Which of the following is a primary mediator of Type I hypersensitivity reactions?

What is the typical duration of the late phase in Type I hypersensitivity reactions?

Which molecules are produced before degranulation and are stored in the granules?

Platelet-activating factor is a primary mediator of Type I hypersensitivity reactions.

The late phase of Type I hypersensitivity reactions typically lasts for less than 6 hours.

IgE cross-linkage does not play a role in initiating degranulation in mast cells and basophils.

What is the primary component of granules in mast cells accounting for about 10% of granule weight?

What biological effects are observed within minutes due to the preformed storage of a particular substance in mast cell granules?

Which molecule is formed before degranulation and is stored in mast cell granules?

What results from the release of histamine from mast cell granules?

What is the primary role of leukotrienes and prostaglandins in the immune response?

What cytokines are secreted by human mast cells, altering the local microenvironment?

What type of hypersensitivity reaction is initiated by nonparasitic antigens known as allergens?

Which effector molecules are more pronounced and longer lasting than histamine in their biological effects?

Leukotrienes and prostaglandins are formed before mast cell degranulation.

Cytokines secreted by human mast cells alter the local microenvironment, leading to the recruitment of inflammatory cells.

The late phase of Type I hypersensitivity reactions typically lasts for more than 6 hours.

Platelet-activating factor is a primary mediator of Type I hypersensitivity reactions.

What is the primary characteristic of systemic anaphylaxis?

What results from anaphylactic shock in systemic anaphylaxis?

What could happen if the allergen in systemic anaphylaxis is inhaled or ingested?

What triggers anaphylactic shock when the allergen enters through the skin in systemic anaphylaxis?

Which of the following is a common cause or trigger for systemic anaphylaxis?

What is the primary outcome of anaphylactic shock in systemic anaphylaxis?

Type 1 hypersensitivity reactions can be systemic or localized.

Anaphylactic shock in systemic anaphylaxis can lead to suffocation if the allergen is inhaled or ingested.

The primary role of leukotrienes and prostaglandins in the immune response is to induce a localized inflammatory response to eliminate antigen without extensively damaging the host's tissue.

What is the term for localized hypersensitivity reactions, usually involving the epithelial surface of the site of allergen entry?

Which condition is triggered by degranulation of mast cells in the lower respiratory tract, leading to early and late responses involving various mediators and inflammatory cells?

Which molecule recruits inflammatory cells, including eosinophils and neutrophils, into the bronchial tissue during the late response of an asthmatic reaction?

Which type of asthma attack can be induced by exercise or cold, independently of allergen stimulation?

What is the primary characteristic of systemic anaphylaxis?

Which molecule is released from mast cell granules and leads to bronchoconstriction, vasodilation, and mucus buildup during the early response of an asthmatic reaction?

Allergic Rhinitis is commonly known as 'hay fever'.

Allergic asthma is triggered by degranulation of mast cells in the nasal mucosa.

The late response of allergic asthma involves the release of additional mediators such as IL-4, IL-5, and TNF-α.

What symptom can be induced by allergen crosslinking of IgE on mast cells along the gastrointestinal tract?

Which cells increase the permeability of mucous membranes, allowing the allergen to enter the bloodstream?

What skin condition is frequently associated with a family history of atopy?

What cells are found in the skin lesions of atopic dermatitis?

Mast cell degranulation along the gut can increase the permeability of mucous membranes, allowing the allergen to enter the bloodstream.

Atopic dermatitis is commonly associated with a family history of atopy.

The skin lesions in atopic dermatitis contain Th 1 cells and a decreased number of eosinophils.

How is Type I hypersensitivity commonly identified and assessed?

What can result from allergen crosslinking of IgE on mast cells along the gastrointestinal tract?

What is the primary role of leukotrienes and prostaglandins in the immune response?

What is the term for the hereditary predisposition to development of immediate hypersensitivity reactions to common environmental antigens?

Mast cell degranulation and the release of histamine and other mediators produce a wheal and flare within 30 minutes in Type I hypersensitivity reactions.

The radio immunosorbent test (RIST) is used to determine the serum level of total IgE antibody in Type I hypersensitivity reactions.

Allergic Rhinitis is commonly known as 'hay fever'.

How can type I hypersensitivities be controlled?

What is the goal of oral immunotherapy (OIT)?

How does Omalizumab work in controlling type I hypersensitivities?

What is the mechanism of action of subcutaneous immunotherapy?

Immunotherapy for type I hypersensitivities includes desensitization, which involves subcutaneous injections of allergens to shift to IgG production instead of IgE.

Oral immunotherapy (OIT) involves feeding children gradually increasing doses of food allergens, with the goal of establishing desensitization.

Monoclonal anti-human IgE, such as Omalizumab, prevents IgE from binding to FcεRI and triggering mast cell degranulation.