Asthma Immunology Quiz

<p>TNFα (B)</p> Signup and view all the answers

<p>Lung tissue (B)</p> Signup and view all the answers

<p>Antibodies (D)</p> Signup and view all the answers

<p>Airway inflammation (A)</p> Signup and view all the answers

<p>Suppresses Th2 response (D)</p> Signup and view all the answers

<p>To secrete antibodies specific to an antigen (C)</p> Signup and view all the answers

<p>IL-4 and IL-13 (D)</p> Signup and view all the answers

<p>Type of infiltrating immune cells (D)</p> Signup and view all the answers

<p>Modifies the constant region while maintaining antigen specificity (D)</p> Signup and view all the answers

<p>They primarily serve as anti-inflammatory therapy for asthma (D)</p> Signup and view all the answers

<p>Asthmatics can have significantly higher IgE levels than non-asthmatics (B)</p> Signup and view all the answers

<p>The arrangement of heavy chain genes involved in antibody classes (C)</p> Signup and view all the answers

<p>Neutrophil infiltration in airways (A)</p> Signup and view all the answers

<p>Histamine (B)</p> Signup and view all the answers

<p>H1 - Gqα, H2 - Gsα, H3 - Giα, H4 - Giα (B)</p> Signup and view all the answers

<p>Cysteinyl leukotrienes (LTC4, LTD4, LTE4) (A)</p> Signup and view all the answers

<p>They mediate the effects of cysteinyl leukotrienes. (D)</p> Signup and view all the answers

<p>Eicosanoids (A)</p> Signup and view all the answers

<p>It is formed into LTB4 or cysteinyl leukotrienes. (B)</p> Signup and view all the answers

<p>IL-4, IL-5, IL-13 (D)</p> Signup and view all the answers

<p>It helps in the conversion of arachidonic acid into LTA4. (A)</p> Signup and view all the answers

<p>IL-1β and TNFα (B)</p> Signup and view all the answers

<p>It contributes to the development of steroid insensitivity. (A)</p> Signup and view all the answers

<p>Up-regulation of Glucocorticoid Receptor β (B)</p> Signup and view all the answers

<p>They are important factors in the disease state producing insensitivity. (B)</p> Signup and view all the answers

<p>It provides superior asthma control compared to glucocorticoid monotherapy. (C)</p> Signup and view all the answers

<p>They are involved in defective glucocorticoid receptor binding. (B)</p> Signup and view all the answers

<p>They improve symptom control and reduce exacerbation rates. (B)</p> Signup and view all the answers

<p>Reduced effectiveness of corticosteroid therapy. (C)</p> Signup and view all the answers

<p>5-LO (D)</p> Signup and view all the answers

<p>Helper T-cells (C)</p> Signup and view all the answers

<p>Interleukin-4 and Interleukin-5 (A)</p> Signup and view all the answers

<p>Destruction of parasites (B)</p> Signup and view all the answers

<p>Allergic responses and asthma severity (A)</p> Signup and view all the answers

<p>Major basic protein (MBP) (A)</p> Signup and view all the answers

<p>CysLTR1 (A)</p> Signup and view all the answers

<p>Higher eosinophil counts correlate with increased severity (B)</p> Signup and view all the answers

<p>Improve phagocytosis of bacteria (D)</p> Signup and view all the answers

<p>Increased intracellular calcium levels (C)</p> Signup and view all the answers

<p>It is recruited to promoters of inflammatory genes. (C)</p> Signup and view all the answers

<p>Only a few genes possess nGREs and are not pro-inflammatory. (B)</p> Signup and view all the answers

<p>It increases gene transcription. (C)</p> Signup and view all the answers

<p>Only a small number of genes have nGREs. (D)</p> Signup and view all the answers

<p>Corticosteroids can induce hundreds of genes with anti-inflammatory potential. (A)</p> Signup and view all the answers

<p>They can overlap binding sites of essential transcription machinery. (D)</p> Signup and view all the answers

<p>Recruiting transcription factors to downregulate inflammatory genes. (C)</p> Signup and view all the answers

<p>IL-10 (B)</p> Signup and view all the answers

The release of pre-formed molecules, like histamine, from mast cells triggered by an external stimulus.

Narrowing of the airways in the lungs, often a symptom of allergic reactions.

A chemical that causes bronchoconstriction and inflammation.

A group of inflammatory chemicals that cause bronchospasm (narrowing of airways) and other responses.

An enzyme that plays a key role in the formation of leukotrienes.

The process by which leukotrienes are made from arachidonic acid using 5-lipoxygenas (5-LO).

A type of histamine receptor that plays a role in the allergic response, influencing smooth muscle cells.

The H1 receptor, a G protein-coupled receptor linked to Gqα, is involved in allergic reactions.

These drugs block the CysLTR1 receptor to prevent bronchoconstriction.

This enzyme converts 5-HETE into LTA4, a precursor to leukotrienes.

An imbalance in Th1 and Th2 cells, with Th2 being higher than normal, linked with allergies and asthma.

Immune cells that attack parasites and contribute to inflammation in asthma.

Eosinophils release substances like ECP, EDN, MBP, and peroxidase, causing inflammation and tissue damage.

An organ where T-lymphocytes mature.

White blood cells with different functions (e.g. helper, cytotoxic, regulatory).

Types of Helper T cells involved in immune responses.

T cells that control and dampen the immune response.

T cells that kill infected or cancerous cells.

A B lymphocyte that has not yet been activated by an antigen. It expresses membrane-bound antibodies that act as its B cell receptor.

A fully differentiated B cell that secretes large quantities of antibodies specific to a particular antigen.

A process where B cells change the type of antibody they produce, while maintaining the same antigen specificity.

An antibody that plays a crucial role in allergic reactions, binding to mast cells and eosinophils.

These white blood cells contribute to asthma inflammation, often found in the airways of mild to moderate asthma patients.

These white blood cells infiltrate the airways of severe asthmatics who don't respond to corticosteroids.

A cornerstone therapy for asthma that effectively reduces inflammation, improving lung function.

Hypochlorous acid, a powerful oxidizing agent produced by macrophages, is vital for killing pathogens but can damage lung tissue if released inappropriately.

A type of macrophage that resides in the alveoli of the lungs, acting as a primary defense against pathogens and removing cellular debris.

In asthma, macrophages exhibit a 'double-edged sword' effect, releasing both pro-inflammatory and anti-inflammatory mediators, contributing to both disease progression and its control.

An anti-inflammatory cytokine released by macrophages in asthma, helping to suppress inflammatory responses and promote healing.

A pro-inflammatory cytokine released by macrophages in asthma, contributing to airway hyperresponsiveness and inflammation in the lungs.

A group of highly reactive molecules released by macrophages, including superoxide anion, hydrogen peroxide, and hydroxyl radical. They play a role in both antimicrobial defense and chronic lung injury.

These proteins, like TNFα, IL-1β, IL-8, are released by macrophages and contribute to inflammation in the lungs, potentially aggravating asthma.

Activated B cells differentiate into antibody-secreting cells, which release antibodies like IgE, playing a role in allergic responses and worsening asthma symptoms.

DNA sequences that overlap with essential transcription factor binding sites, preventing the activation of certain genes by glucocorticoid receptors (GR).

nGREs inhibit gene transcription by physically blocking the binding of essential transcription factors to their target sites, thus preventing the assembly of the transcription machinery and gene activation.

Genomic analysis reveals that only a small number of genes contain nGREs, and those genes are typically NOT pro-inflammatory. Therefore, nGREs alone cannot account for the broad anti-inflammatory effects of corticosteroids.

Acetylation of histone tails enhances the accessibility of DNA to transcription factors, leading to increased gene transcription.

Deacetylation of histone tails reduces the accessibility of DNA to transcription factors, leading to decreased gene transcription.

Corticosteroids induce the recruitment of histone deacetylase 2 (HDAC2) to the promoters of inflammatory genes, leading to their deacetylation and repression of transcription.

Corticosteroids induce the expression of hundreds of genes, many of which have anti-inflammatory properties, through the recruitment of HDAC2 and other mechanisms.

The anti-inflammatory effects of corticosteroids involve multiple mechanisms, making it difficult to pinpoint a single key mediator. This redundancy ensures a robust and reliable therapeutic effect.

Smoking impairs corticosteroid efficacy by promoting inflammation and hindering their anti-inflammatory actions.

Insensitivity can arise due to reduced glucocorticoid receptor expression, increased dominant negative receptor isoforms, and inhibition of key transcription factors that mediate steroid actions.

Infections, especially those caused by viruses, can impair corticosteroid efficacy by activating inflammatory pathways and interfering with receptor signaling.

The balance of different immune cells, particularly the reduction of regulatory T cells and an increase in pro-inflammatory cells, can contribute to corticosteroid insensitivity.

By stimulating the β2-adrenergic receptor in the airways, LABAs improve bronchodilation and synergize with corticosteroids in suppressing inflammation.

LABAs, PDE inhibitors, and other agents that modulate inflammatory pathways can reduce the need for high doses of corticosteroids, minimizing side effects.

This study demonstrated the superiority of combining a LABA with a corticosteroid over increasing the corticosteroid dose alone in managing asthma, leading to widespread use of these combinations.

These pumps, like P-glycoprotein, can export corticosteroids from cells, reducing their intracellular concentration and efficacy.