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I have been part of the field of immunology for the past fifteen years. Previously, my studies were focused on researching the anti-inflammatory properties of the acute phase protein α-1-antitrypsin (AAT) in the context of acute inflammatory responses post transplantation mediated by damage associated molecular patterns (DAMPs). These inflammatory responses can also be associated with autoinflammatory and autoimmune conditions. Specifically, I investigated the cellular events which lead to the extracellular presence of DAMP, in addition to examining the proinflammatory effect of three specific DAMP molecules: 1. Heat shock proteins (HSPs), gp96 and HSP70 and 2. the histone like protein high mobility group box 1 (HMGB1). For example, in a previous report we demonstrated that human AAT (hAAT) inhibits extracellular gp96 inflammatory mediated responses in vivo and in vitro. Furthermore, we showed that hAAT regulated the immune response during a bacterial infection (Kaner and Ochayon et al. J. Infec Dis,2015). In addition, I was involved in several studies demonstrating hAAT immune-regulatory behavior. I have investigated the role of the inflammatory response in animal models associated with allogeneic and syngeneic transplantation, vaccination, and bacterial infection. My training continued as post graduate fellow, I have expanded my experimental horizons and examined the inflammatory milieu associated with vaccine response (under the guidance of Dr. Waggoner). I questioned the role of mixed inflammatory environment which characterizes respiratory conditions such as severe asthma and COPD on NK cells functionality. Specifically, we investigated how a combination of type 1 (IL-12) and type 2 (IL-33) cytokines contribute to an enhanced cytokine production by human NK cells, we also showed that molecular mechanism which enabled this responses was via p38 MAPK pathway as well as ATF2 (Ochayon et al. JLB, 2020). Subsequently, my training continues in the Asthma division at CCHMC under the guidance of Dr. Hershey. Since early life occurrence of atopic dermatitis (AD) is strongly associated with the prevalence of childhood asthma. As part of the MPAACH cohort we are currently examining the phenotype of NK and T cells in addition to participants clinical data. Recently, we reported that NK cells derived from AD patients with allergen sensitized compared to non-allergen sensitized showed reduced expression of NKG2D at subsequent clinical visits. In addition, NK cells derived from allergen sensitized children showed reduced cytotoxicity and hyper-inflammatory behavior characterized by increased expression of TNF-alpha. There are additional ongoing studies associated to the role of NK cells in childhood AD and asthma, in addition to the effect of non-canonical cytokine combinations on NK cells functionality.