A photo of Ian Lewkowich.

Assistant Professor, UC Department of Pediatrics


Biography & Affiliation


While Th2 immune responses are central to disease pathology in allergic asthma, there is a growing understanding that the Th2 paradigm is not sufficient to explain the entire spectrum of disease severity. Indeed, there is growing belief that severe disease may be driven by a different process than mild to 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. We have found that the development of severe allergic asthma is associated with a limited capacity of Tregs to limit pulmonary dendritic cell activity, enhanced capacity for antigen uptake by pulmonary myeloid dendritic cells, and the development of a mixed Th2/Th17 immune response. In contrast, C3H mice demonstrate increased Treg activity, preferential antigen uptake by pulmonary plasmacytoid dendritic cells, and an exclusively Th2-biased immune response. We are presently using the A/J versus C3H/HeJ mouse model of allergic asthma to tease out the mechanisms responsible the development of severe allergic asthma.

Academic Affiliation

Assistant Professor, UC Department of Pediatrics




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


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.