Immune modulation and the role of innate immune cells in allergy and asthma

Peanut allergy is the most common foodrelated source of an anaphylactic reaction.1 Prevalence of peanut allergy varies considerably by region, but in some highincome countries an estimated 0.2%– 2.5% of children are affected.2 Many studies are exploring potential peanutspecific immunotherapy approaches and one oral immunotherapy treatment has been FDA approved for treatment. To address the need for more effective peanut allergy treatments, Angelina et al.3 investigated the immunomodulation properties of the nonspecific, synthetic cannabinoid molecule, WIN552122, on peanutstimulated dendritic cells (DCs). Human monocytederived dendritic cells (hmoDCs) from healthy donors were stimulated with crude peanut extract (CPE) alone or WIN552122. CPEstimulated hmoDCs activated T cells that produce significantly higher levels of IL5 compared to unstimulated hmoDCs, with no significant changes in IFNγ and IL10. Interestingly, in the presence of WIN552122, T cells secreted significantly lower levels of IFNγ and IL5 and considerably higher levels of IL10 (Figure 1). Additionally, a preclinical model of peanutallergic sensitization was used to assess the ability of WIN552122 to impair peanutinduced DC migration from skin to lymph nodes. BALB/c mice were subjected to CPE sensitization for 3 days with the presence or absence of WIN552122, followed by characterizing the frequency and activation status of DCs in draining lymph nodes. The presence of WIN552122 along CPE sensitization showed a reduction in the migration of DCs to the lymph node and significantly lower numbers of mature DCs. The study findings confirm that WIN552122 shifts the peanutstimulated human DCs from proallergic to tolerogenic responses. It also showed that it is achieved by polarizing TH2 response while increasing IL10 producing CD4+ T cells and FOXP3+ Treg cells. These novel findings may facilitate the development of future novel therapeutic and prophylactic approaches for peanut allergy. Viral respiratory infections, particularly rhinoviruses, are the most prominent trigger of asthma exacerbations.4 Rhinoviruses were shown to induce airway inflammation and worsen clinical symptoms, with increased exacerbation risk for viral infection concurring with allergen exposure for asthmatic patients.5 Although the role of DCs is well established in both viral infections and allergens,6 little is known about their role in viral asthma exacerbations. Cameron et al.7 address this issue by characterizing DC populations in lower airways in moderately severe asthmatic patients in healthy controls. The asthmatic subjects and healthy controls were infected with the rhinovirus (RVA16), with both groups underwent bronchoscopies and bronchoalveolar lavage at baseline (day14), day 3 and day 8 postinfection. The main observation was that at the lower airways,