Division of mastocytoses according to updated WHO Classification is clinically relevant. Overall survival is worse in indolent systemic mastocytosis compared to cutaneous mastocytosis. Trephine biopsy is necessary to distinguish indolent systemic mastocytosis from cutaneous mastocytosis.

Maternal intake of α-linolenic acid increased ω3 DPA and its 14-lipoxygenation products in the breast milk of dams. 14-lipoxygenation products of ω3 DPA increased TRAIL expression on plasmacytoid dendritic cells in the pups, which suppressed the IFN-γ-producing T cells and consequently inhibited infant allergic dermatitis.

Electron microscopy and solution scattering reveal that the structure of entire IgE is highly rigid with a spatial organization differing from current models. The Fab arms are rigidly tethered to the Fc and lack flexibility. Ligelizumab traps IgE in an extended conformation retaining the Fab arm assembly. The localization of the epitope enables inhibition of binding to both IgE receptors.

Short-chain fatty acids suppress primary human mast cell activation via HDAC inhibition and not via PPAR or GPR signaling. Butyrate induces transcriptional changes of genes important for signaling and activation of human mast cells. Butyrate triggers a redistribution of global H3K27 acetylation levels, leading to decreased acetylation at the transcription start site of genes encoding key FcεRI-mediated signaling molecules.

Asthmatics patients with high level of CD66⁺ neutrophils have high C16:0 ceramide levels and enhanced ceramide-mediated pro-apoptotic signals (BID and JNK). Asthmatics patients with high level of platelet-adherent eosinophils (CD61⁺ platelets/Siglec8⁺ eosinophils) have high S1P levels. The level of CD66⁺ neutrophils correlates with ROS production from neutrophils. The level of platelet-adherent eosinophils is associated with asthma control symptom scores.

Early-life rhinovirus infection increases epithelial expression of the innate cytokines IL-25 and IL-33, expands (type 2 innate lymphoid cells) ILC2s, and enhances development of an asthma-like phenotype. Rhinovirus causes macrophage (NLR family, pyrin domain containing 3) NLRP3 inflammasome activation and bioactive IL-1β production. IL-1β production, which is deficient in immature mice, attenuates production of IL-25 and IL-33, thereby protecting against rhinovirus-induced asthma development.

This study presents data from a large cohort of infants at risk for atopy. Effect of orally applied bacterial lysates during infancy on later allergic manifestations was studied in a long prospective follow-up. The early intervention with a bacterial lysate had no effect on the development of atopic dermatitis, allergic rhinitis, asthma and specific sensitization to aeroallergens at school age.

This randomized, double-blind, placebo-controlled phase III clinical trial demonstrates the efficacy and favourable safety profile of the 32-week SLIT with Artemisia annua in patients with seasonal allergic rhinitis. Artemisia annua-SLIT significantly reduces total nasal symptom score at the 1st and 2nd PPP compared with placebo. Preseasonal Artemisia annua-SLIT significantly decreases Th2 cells, increases nTreg and Tr1 cells in blood and increases CST1 in nasal secretion.

Although the sinus microbiome is highly variable between individuals, we identify a core microbiome comprised of Corynebacterium, Staphylococcus, Streptococcus, Haemophilus and Moraxella species in both healthy and chronic rhinosinusitis cohorts. Amongst patients suffering from chronic rhinosinusitis with nasal polyps, a statistically significant reduction in relative abundance of Corynebacterium was identified. Despite some measured differences in microbiome composition between participating centres in our cohort, these differences would not alter the general pattern of core organisms described above.

In this retrospective, real-world study in Germany, effectiveness of (allergen immunotherapy) AIT with a subcutaneous (house dust mite) HDM allergoid was analyzed in comparison with a non-AIT control group. After up to 6 years of follow-up, the probability of asthma development in patients treated with HDM allergoid was significantly lower compared to the control group. Patients treated with HDM allergoid required significantly fewer medications for allergic rhinitis and asthma, thus indicating the preventive effect of HDM allergoid AIT on asthma occurrence and progression.