The underlying mechanism of allergic rhinitis involves IgE antibodies attaching to the allergen and causing the release of inflammatory chemicals such as histamine from mast cells. Cytokines are very important in this process. Many data suggest a systemic shift to more intensely type 1-dominated immune responses in non-allergic individuals and, conversely, to more type 2-dominated responses in allergic individuals upon natural re-exposure to grass pollen. However other studies have found that chemokine (C-X-C motif) ligand (CXCL) 10/interferon (IFN)-gamma-induced protein 10 (IP-10) and CXCL9/monokine induced by IFN-gamma (MIG) concentrations are elevated in nasal lavages from allergic patients suggesting that these chemokines may play a role in chronic allergic inflammation. Several studies have also evaluated the effect of different immune-modulating drugs in allergic rhinitis showing local and peripheral increase of IFN-gamma and IP-10, associated with a reduction of symptoms. Further studies are needed to clarify the role of T helper (Th) 1 chemokines in the pathogenesis of allergic rhinitis, and to evaluate their role as biomarkers of disease and of response to treatments.