100+ Free CMSA Diploma in Allergology Dip Allerg(SA) Practice Questions

Explanation: The high-affinity IgE receptor (FcεRI) on mast cells and basophils is a tetrameric complex composed of one IgE-binding alpha (α) chain, one signal-amplifying beta (β) chain, and a disulfide-linked gamma (γ2) homodimer. Signal transduction relies on ITAMs located on the cytoplasmic tails of both the β chain and the γ chains, which become phosphorylated by Lyn kinase upon antigen-mediated receptor cross-linking.

Explanation: Interleukin-4 (IL-4) and Interleukin-13 (IL-13) bind to heterodimeric IL-4 receptor complexes on B cells, triggering Janus kinase (JAK1/JAK3) activation and phosphorylation of Signal Transducer and Activator of Transcription 6 (STAT6). Phosphorylated STAT6 homodimers translocate to the nucleus to activate germline Cε transcription, directing immunoglobulin class switch recombination to IgE.

Explanation: Histamine, tryptase, chymase, carboxypeptidase A3, and heparin are preformed mediators packaged within ionic complexes inside mast cell secretory granules, released within minutes of degranulation. In contrast, LTC4 and PGD2 are newly synthesized lipid mediators produced via arachidonic acid metabolism, and cytokines like IL-13 are synthesized de novo over hours.

Explanation: Type I (immediate) hypersensitivity is mediated by allergen binding to specific IgE antibodies bound to FcεRI receptors on mast cells and basophils, resulting in rapid degranulation and release of histamine, leukotrienes, and prostaglandins within minutes of exposure.

Explanation: Regulatory T cells (Tregs) are characterized by surface expression of CD4 and high-affinity IL-2 receptor alpha chain (CD25), alongside expression of the master transcription factor Forkhead Box P3 (FoxP3). Tregs maintain allergen tolerance by secreting immunosuppressive cytokines (IL-10 and TGF-β) and expressing CTLA-4 to downregulate co-stimulatory molecules on antigen-presenting cells.

Explanation: CCR3 is a G-protein coupled receptor abundantly expressed on eosinophils (as well as basophils and Th2 cells). It acts as the primary receptor for the eotaxin family (CCL11, CCL24, CCL26) and RANTES (CCL5), driving selective recruitment and transendothelial migration of eosinophils into inflamed allergic tissues.

Explanation: Thymic Stromal Lymphopoietin (TSLP), Interleukin-33 (IL-33), and Interleukin-25 (IL-25 / IL-17E) are epithelial-derived cytokines released in response to barrier disruption, proteases, or micro-organisms. They directly stimulate ILC2s via ST2 (IL-33R), IL-17RB (IL-25R), and TSLPR, triggering antigen-independent secretion of massive amounts of IL-5 and IL-13.

Explanation: C3a and C5a (and to a lesser extent C4a) are small peptide fragments generated during complement cascade activation. They function as anaphylatoxins that bind specific receptors (C3aR and C5aR/CD88) on mast cells, basophils, and granulocytes, stimulating smooth muscle contraction, vascular permeability, and mast cell degranulation via non-IgE mechanisms.

Explanation: FcεRII (CD23) is a transmembrane C-type (calcium-dependent) lectin protein, distinguishing it from most Fc receptors which belong to the immunoglobulin superfamily. It exists in membrane-bound and soluble forms (sCD23) on B cells, macrophages, and follicular dendritic cells, playing key roles in regulating IgE synthesis and IgE-mediated antigen presentation.

Explanation: Histamine H1 receptors are Gq/11-protein coupled receptors. Receptor binding activates Phospholipase C (PLC), which cleaves phosphatidylinositol 4,5-bisphosphate (PIP2) into inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG). IP3 triggers calcium release from the endoplasmic reticulum, leading to endothelial cell contraction, intercellular gap formation, and tissue edema.