Ans. is 'a' i.e., Type -1 Pathogenesis of allergic rhinitiso Allergic rhinitis is a type I hypersensitivityIt occurs in two phases:-1) Initial response/Acute or early phase# After first antigen exposure, this antigen is presented to CD-4 helper T cells (TH, type) by antigen presenting cells. These primed TH, cells release IL-4 that acts on B-cells to form Ig E specific for that particular antigen. The antigen specific Ig E antibodies then bind to the surface receptors of mast cells and basophils. The process from first antigen exposure to the coating of mast cells by Ig E acts as sensitization (prior sensitization) and first exposure is also called priming or sensitizing exposure (dose). Subsequent exposure (shocking dose) to same antigen then results in activation of mast cells and basophils with release of inflammatory mediators : -i) Histamine (most important)ii) Hepariniii) Leukotriens (B4, C4> D4)iv) PGD2v) PAFvi) Cytokines (IL-1, 3, 4, 5, 6; INF)vii) Eosinophil chemolactic factor (ECF)viii) Neutrophil chemolactic factor (NCF)The release of these mediators result in : -Increased vascular permeability and vasodilatation which result in tissue edema - Nasal blockage and sneezing.Smooth muscle spasm - BronchoconstrictionHyperactivity of glands - RhinorrheaRecruitment of inflammatory cells.2) Late phase responseRecruited inflammatory cells of initial phase amplify and sustain the inflammatory response without additional exposure to the triggered antigen. PAF is the most important mediator in initiation of late phase response. Eosinophils are particularly important cells among the recruited cells which also include neutrophils, basophils, monocytes and T-cells. It causes symptoms like nasal congestion and post nasal drip.