A photo of Ian Lewkowich.

Assistant Professor, UC Department of Pediatrics

513-636-3999

Biography & Affiliation

Biography

I have always been interested in the immune system. Allergic diseases and the immune response are particularly fascinating to me.

In allergic diseases, the immune system responds to things that it shouldn't, like dust or an allergen from a pet. While everyone is exposed to these substances in our homes or workplaces, not everyone is allergic. Determining why some people are allergic and others are not was the hook that got me interested in this field.

In my lab, we are working on determining what causes the development of severe allergic asthma as opposed to mild or moderate forms of the disease, which are more amenable to therapeutic interventions. We are focused on establishing how exposure in early life (including in utero) influences allergic asthma development.

Notably, we have demonstrated that the production of additional factors associated with severe allergic asthma synergizes with factors produced in mild/moderate disease.

Using a mouse model of allergic asthma in which one strain develops a phenotype characteristic of mild asthma (C3H/HeJ) and others develop a phenotype characteristic of severe disease (A/J), we have identified several novel mechanisms through which asthma severity is regulated.

The National Institutes of Health has continuously funded my research since 2012.

Academic Affiliation

Assistant Professor, UC Department of Pediatrics

Research Divisions

Immunobiology

Education

PhD: University of Manitoba, Winnipeg, Canada, 2004.

Publications

Insulin-like Growth Factor 1 Supports a Pulmonary Niche that Promotes Type 3 Innate Lymphoid Cell Development in Newborn Lungs. Oherle, K; Acker, E; Bonfield, M; Wang, T; Gray, J; Lang, I; Bridges, J; Lewkowich, I; Xu, Y; Ahlfeld, S; et al. Immunity. 2020; 52:275-294.e9.

Age and early maternal smoking contribute to epithelial cell IL-13 responsiveness in a pediatric asthma population. McAlees, JW; Baker, T; Kaur, D; McKnight, C; Lindsley, A; Strait, RT; Zhang, X; Myers, JM B; Kovacic, MB; Lewkowich, IP. Allergy: European Journal of Allergy and Clinical Immunology. 2019; 74:2485-2488.

Immunomodulatory T cell death associated gene-8 (TDAG8) receptor in depression-associated behaviors. McMurray, KM J; Vollmer, LL; Ahlbrand, R; Thomas, J; Winter, A; Lewkowich, IP; Sah, R. Physiology and Behavior. 2019; 209:112598-112598.

RAGE-induced asthma: A role for the receptor for advanced glycation end-products in promoting allergic airway disease. Brandt, EB; Lewkowich, IP. Journal of Allergy and Clinical Immunology. 2019; 144:651-653.

Short-term high-fat diet feeding protects from the development of experimental allergic asthma in mice. Schroeder, T; Wiese, AV; Ender, F; Quell, KM; Vollbrandt, T; Duhn, J; Suenderhauf, A; Kuenstner, A; Moreno-Fernandez, ME; Derer, S; et al. Clinical and Experimental Allergy. 2019; 49:1245-1257.

Combined administration of anti-IL-13 and anti-IL-17A at individually sub-therapeutic doses limits asthma-like symptoms in a mouse model of Th2/Th17 high asthma. Kim, D; McAlees, JW; Bischoff, LJ; Kaur, D; Houshel, LK; Gray, J; Hargis, J; Davis, X; Dudas, PL; Deshmukh, H; et al. Clinical and Experimental Allergy. 2019; 49:317-330.

Loss of GTPase of immunity-associated protein 5 (Gimap5) promotes pathogenic CD4(+) T-cell development and allergic airway disease. Patterson, AR; Bolcas, P; Lampe, K; Cantrell, R; Ruff, B; Lewkowich, I; Hogan, SP; Janssen, EM; Bleesing, J; Hershey, GK K; et al. Journal of Allergy and Clinical Immunology. 2019; 143:245-257.e6.

C3a is required for ILC2 function in allergic airway inflammation. Gour, N; Smole, U; Yong, H; Lewkowich, IP; Yao, N; Singh, A; Gabrielson, E; Wills-Karp, M; Lajoie, S. Mucosal Immunology. 2018; 11:1653-1662.

Distribution and Interaction of Murine Pulmonary Phagocytes in the Naive and Allergic Lung. Hoffmann, FM; Berger, JL; Lingel, I; Laumonnier, Y; Lewkowich, IP; Schmudde, I; Koenig, P. Frontiers in Immunology. 2018; 9.

TSLP signaling in CD4(+) T cells programs a pathogenic T helper 2 cell state. Rochman, Y; Dienger-Stambaugh, K; Richgels, PK; Lewkowich, IP; Kartashov, AV; Barski, A; Hershey, GK K; Leonard, WJ; Singh, H. Science Signaling. 2018; 11:eaam8858-eaam8858.