Asthma is a heterogenous immunological condition usually characterized by a chronic airway inflammation, with different underlying disease processes. It is defined by the history of respiratory symptoms such as wheeze, shortness of breath, chest tightness and cough that vary over time and in intensity, together with variable expiratory airflow limitation [1], [2], [3]. Asthma is a common chronic respiratory disease affecting 1 to 18 % of the general population depending on the country [4], [5]. The prevalence of asthma in childhood is elevate and up to 7 % of adolescents had severe asthma symptoms [5].

It is currently accepted that the term asthma refers to several conditions with distinct mechanistic pathways (endotypes) and variable clinical presentations (phenotypes) [6]. This is why a better understanding of the immune mechanisms involved in each endotype is crucial to the management of asthma [7], [8]. Severe asthma (SA) affects 2 % to 5 % of children with asthma. Children with SA (cwSA) suffer from frequent exacerbations despite being treated with inhaled corticosteroids and at least another controller, good treatment adherence and technique and removal of environmental factor such as tobacco [9], [10]. CwSA have a reduced quality of life. Association between asthma and other atopic conditions such as atopic dermatitis (AD) was described in children [5], [11]. AD, also known as eczema and atopic eczema, is one of the most common inflammatory disorders characterized by intense itching and recurrent eczematous lesions [5], [12]. AD affects up to 20 % of children and 10 % of adults in high-income countries [5], [13], [14]. Previous studies described the progression of atopic disorders from AD in infants to allergic rhinitis and asthma in children [15], [16]. In addition, it was reported that up to 25 % of children with current AD also have asthma [17].

Asthma and AD share common genetic and immunological features [18], [19]. These two pathologies were originally considered to be mediated by an imbalance towards a T helper 2 (Th2) and exaggerated IgE responses to allergens [7], [11], [12], [19], [20]. In this context, biologics such as dupilumab (anti-IL-4Ra) and omalizumab (anti-IgE) are effective treatments of moderate to severe asthma and AD [21], [22], [23]. However, not all cwSA have AD, and clinical responses to biologics may vary among cwSA, children with AD or both [24]. In addition, it remains unclear whether cwSA with current AD and cwSA without AD have distinct local and systemic immune profile. Here, we carried out an in-depth analysis of the immune profile of cwSA according to the presence or absence of AD to determine the main immune features they share and those that distinguish them. For this, we analyzed distinct T cell populations, including innate-like T (ILT) cells as mucosal-associated invariant T (MAIT), invariant Natural Killer T (iNKT) and γδ T cells [25], [26], [27], [28], and cytokine levels in both bronchoalveolar lavage (BAL) and blood from cwSA with current AD and cwSA without AD.