Judith A. Woodfolk, MBChB, PhD

The Woodfolk lab studies the immune response to environmental triggers of allergic and respiratory diseases.

We use translational models to understand how immune cells respond to viruses and allergens in health and disease. Our overarching goal is to identify biomarkers that can predict severe outcomes in at-risk patients, and identify new strategies to prevent and treat disease.

A major focus is to advance knowledge on how respiratory viruses worsen asthma and contribute to chronic airway inflammation. Infection with rhinovirus, the major cause of common cold, typically runs a benign course. However, in patients with allergic asthma, rhinovirus exposure triggers acute wheezing episodes that often require hospitalization. We have characterized T cells and B cells that constitute a protective response to rhinovirus, and identified a previously unrecognized role for type 1 immunity in promoting allergic asthma. Current work on rhinovirus seeks to understand the role of novel T cell types in asthma severity. The analytical pipelines developed for rhinovirus have since laid the groundwork for defining how the immune response contributes to chronic inflammation in patients suffering from post-acute sequelae of COVID-19. Additional initiatives in the lab focus on emerging allergic disorders, including elucidating immune responses governing allergy to mammalian meat and eosinophilic esophagitis.

Our systems biology methods use an inter-disciplinary approach to integrate clinical features of disease with immune data generated using state-of-the-art single-cell technologies and novel computational tools. This strategy reveals discrete immunophenotypes that promote disease processes, with the ultimate goal of improving treatments in individual patients.

Recent Relevant Publications

1. Muehling LM, Heymann PW, Carper H, Murphy DD, Rajadhyaksha E, Kennedy J, Early SV, Soto-Quiros M, Avila L, Workman L, Platts-Mills TA, Woodfolk JA. Cluster analysis of nasal cytokines during rhinovirus infection identifies different immunophenotypes in both children and adults with allergic asthma. Clin Exp Allergy. 2022, in press.
2. Barone SM* Paul AG*, Muehling LM*, Lannigan JA, Kwok WW, Turner RB, Woodfolk JA^**, Irish JM^**. Unsupervised machine learning reveals key immune cell subsets in COVID-19, rhinovirus infection, and cancer therapy. 2021 Aug 5;10:e64653. Joint first (*) and co-corresponding (**) authors.
3. Muehling LM, Heymann PW, Wright PW, Eccles JD, Agrawal R, Carper HT, Murphy DD, Workman LJ, Word CR, Ratcliffe SJ, Capaldo BJ, Platts-Mills TA, Turner RB, Kwok WW, Woodfolk JA. Human Th1 and Th2 cells targeting rhinovirus and allergen coordinately promote allergic asthma. J Allergy Clin Immunol. 2020;146:555-570.
4. Heymann PW, Platts-Mills TA, Woodfolk JA, Borish L, Murphy DD, Carper HT, Conaway MR, Steinke JW, Muehling L, Gerald TW, Kennedy JL, Irani AM, McGraw MD, Early SV, Wheatley LM, Adams AP, Turner RB. Understanding the asthmatic response to an experimental rhinovirus infection: Exploring the effects of blocking IgE. J Allergy Clin Immunol. 2020;146:545-554.
5. Eccles JD, Turner RB, Kirk NA, Muehling LM, Borish L, Steinke JW, Payne SC, Wright PW, Thacker D, Lahtinen SJ, Lehtinen MJ, Heymann PW, Woodfolk JA. T-bet+ memory B cells link to local cross-reactive IgG upon human rhinovirus infection. Cell Rep. 2020;30:351-66.
6. Muehling LM, Turner RB, Brown KB, Wright PW, Patrie JT, Lahtinen SJ, Lehtinen MJ, Kwok WW, Woodfolk JA. Single-cell tracking reveals a role for pre-existing CCR5+ memory Th1 cells in the control of rhinovirus-A39 after experimental challenge in humans. J Infect Dis. 2018; 217:381-92.
7. Wisniewski JA*, Muehling LM*, Eccles JD, Capaldo BJ, Agrawal R, Shirley DA, Patrie JT, Workman LJ, Schuyler AJ, Lawrence MG, Teague WG, Woodfolk JA. Th1 signatures are present in the lower airways of children with severe asthma regardless of allergic status. J Allergy Clin Immunol. 2018; 141:2048-60.