Last year brought a significant advance in asthma management, unyielding to the pressure of the pandemics. Novel key findings in asthma pathogenesis focus on the resident cell compartment, epigenetics and the innate immune system. The precision immunology unbiased approach was supplemented with novel tools and greatly facilitated by the use of artificial intelligence. Several randomised clinical trials and good quality realworld evidence shed new light on asthma treatment and supported the revision of several asthma guidelines (GINA, Expert Panel Report 3, ERS/ATS guidelines on severe asthma) and the conception of new ones (EAACI Guidelines for the use of biologicals in severe asthma). Integrating asthma management within the broader context of Planetary Health has been put forward. In this review, recently published articles and clinical trials are summarised and discussed with the goal to provide clinicians and researchers with a concise update on asthma research from a translational perspective.

Immune modulation is a key therapeutic approach for allergic diseases, asthma and autoimmunity. It can be achieved in an antigen‐specific manner via allergen immunotherapy (AIT) or in an endotype‐driven approach using biologicals that target the major pathways of the type 2 (T2) immune response: immunoglobulin (Ig)E, interleukin (IL)‐5 and IL‐4/IL‐13 or non‐type 2 response: anti‐cytokine antibodies and B‐cell depletion via anti‐CD20. Coronavirus disease 2019 (COVID‐19) vaccination provides an excellent opportunity to tackle the global pandemics and is currently being applied in an accelerated rhythm worldwide. The vaccine exerts its effects through immune modulation, induces and amplifies the response against the severe acute respiratory syndrome coronavirus (SARS‐CoV‐2). Thus, as there may be a discernible interference between these treatment modalities, recommendations on how they should be applied in sequence are expected. The European Academy of Allergy and Clinical Immunology (EAACI) assembled an expert panel under its Research and Outreach Committee (ROC). This expert panel evaluated the evidence and have formulated recommendations on the administration of COVID‐19 vaccine in patients with allergic diseases and asthma receiving AIT or biologicals. The panel also formulated recommendations for COVID‐19 vaccine in association with biologicals targeting the type 1 or type 3 immune response. In formulating recommendations, the panel evaluated the mechanisms of COVID‐19 infection, of COVID‐19 vaccine, of AIT and of biologicals and considered the data published for other anti‐infectious vaccines administered concurrently with AIT or biologicals.

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Abstract:Background: Ulcerative colitis (UC) is a chronic inflammatory autoimmune disease with limited treatment modalities. The animal model of colitis induced by treatment with trinitrobenzene sulfonic acid (TNBS-colitis) is commonly used to test new therapies of this disease. In our previous work we found that epicutaneous (EC) immunization with protein antigen induced a state of profound immunosuppression that inhibited inflammatory response in contact sensitivity, in experimental autoimmune encephalomyelitis (EAE) and in allogeneic skin graft rejection. Methods: TNBS-induced colitis was used as an experimental model. Results: In our current work, we showed that EC immunization with TNP-conjugated mouse immunoglobulin (TNP-Ig) prior to induction of TNBS-colitis alleviates disease severity what was determined by the body weight, the length and the weight of the colon, the histological activity index (HAI) and myeloperoxidase activity (MPO). Observed amelioration of the disease in TNP-Ig patched mice was accompanied with decreased production of IFN-g and IL-17A by splenocytes. Additionally, spleen cells isolated from mice EC immunized with TNP-Ig prior to colitis induction showed increased production of IL-10 suggesting that this cytokine might be involved in inhibiting inflammatory response in the colon. Conclusion: This work shows that EC immunization with protein antigen prior to TNBS-colitis induction ameliorates disease and observed suppression of inflammatory response in the colon might be mediated by IL-10.

As we have shown previously that protein antigen applied epicutaneously (EC) in mice inhibits TNP-specific Th1-mediated contact sensitivity (CS), we postulated that the maneuver of EC immunization might also suppress Tc1-dependent CS response. Here we showed that EC immunization of normal mice with 2,4-dinitrophenylated bovine serum albumin (DNP-BSA) applied on the skin in the form of a patch induces a state of subsequent unresponsiveness due to regulatory T cells (Treg) that inhibited sensitization and elicitation of effector T-cell responses. Suppression is transferable in vivo by TCRab + CD4 + CD25 + lymphocytes harvested from lymph nodes (LNs) of skin-patched animals. Flow cytometry revealed that EC immunization with DNP-BSA increased TCRab + CD4 + CD25 + FoxP3 + lymphocytes in subcutaneous LNs, suggesting that observed suppression was mediated by Treg cells. Further, in vitro experiments showed that EC immunization with DNP-BSA prior to 1-fluoro-2,4-dinitrobenzen sensitization suppressed LN cell proliferation and inhibited production of TNF-a, IL-12 and IFN-c. Using a transwell system or anti-CTLA-4 mAb, we found that EC induced suppression required direct Treg-effector cell contact and is CTLA-4-dependent. Contact sensitivity (CS), also known as allergic contact, dermatitis is a serious health problem and one of the most common occupational diseases in developed countries. 1 CS responses to contact-sensitizing haptens, such as picryl chloride, oxazolone or dinitrofluorobenzene (DNFB), are classical manifestations of T-cell-mediated immunity in vivo. In previously sensitized hosts, CS and the related delayed-type hypersensitivity reaction are manifested as macroscopically measurable inflammation (skin swelling) that peaks at 24-48 h after topical cutaneous hapten challenge. 2 CS can be mediated by either CD4 + Th1, MHC class II-restricted cells locally releasing IFN-g to recruit a characteristic inflammatory infiltrate, 2 or CD8 + MHC class I-restricted Tc1 cells, which can similarly release IFN-g but predominately mediate cytotoxic damage to local skin cells, such as keratinocytes, 3,4 and by IL-17-producing Th17 cells. 5 Tc1-mediated CS to DNFB in BALB/c mice also requires participation of B-1, NKT and TCRgd lymphocytes that enable recruitment of Tc1 effector cells. 6 CS response to DNFB is mediated by CD8 + T cells that are regulated by CD4 + T lymphocytes. 7 It was already shown that Tc1-mediated CS to DNFB was negatively regulated by antigen (Ag)-specific CD4 + CD25 + FoxP3 + CTLA-4 T regulatory T cells (Treg), which are induced by hapten skin sensitization. 8 This population of regulatory cells expresses high level of inducible costimulator and are distinguishable from other Treg cells by the expression of IFN-g, IL-10 and IL-17. 8 On the other hand, suppression of Tc1-mediated CS can be induced via gavage with the hapten. 9 This type of hapten immunization induces deletion of a large fraction of Ag-specific CD8 T cells in the liver, and mesenteric lymph nodes (LNs) also trigger the suppressive fu...