Division of Allergy & Immunology

• Stephanie Eisenbarth, MD, PhD
  Co-Program Director 
• Sergejs Berdnikovs, PhD
  Co-Program Director
• Thongsy Singvongsa
  Division Administrator

The following are expected of all trainees accepted into the NUAIR program:

• Dedicate to research more than 75 percent effort, or more than 30 hours per week. Mentors and trainee will monitor trainee's effort load so that they spend more than 30 hours per week in hands-on research, working in the bench or clinical lab.
• Meet the following milestones:
  • Submit an abstract to a national meeting yearly.
  • Submit an application for a K award (internal K, K08, K23 or K99/R00) and a non-NIH application (e.g., medical society, foundation) in the second year.
  • Submit at least one manuscript as first author based on their own research project.
  • Submit at least another manuscript during the two years of research training (co-author in another collaborative work, in a review, in a chapter, etc).
  • For MD trainees: maintain clinical skills and pass the American Board of Allergy and Immunology certifying examination.
  • Apply for an academic position in the second year of training.
  • Actively participate in teaching in the division lectures, didactic activities, and immunology annual retreat.
• Lectures, course work, clinical work, and all other activities must not prevent the trainee from dedicating more than 30 hours per week to hands-on research.
• Trainees attend the following divisional lectures on a weekly basis: Allergy and Immunology Laboratory Meeting (Mondays 12-1 p.m.), Allergy and Immunology journal club (Tuesdays 1:30-2:30 p.m., and Allergy and Immunology research conference (Fridays 12-1 p.m.).
• Trainees attend and present at these annual meetings: Northwestern Immunology Retreat, Autumn Immunology Conference and a national meeting, preferably that of the American Academy of Allergy and Immunology.
• Trainees must participate in the educational and self-improvement activities of the NUAIR program (evaluations, committees, etc.).
• Trainees must be collegial and promote collaborative research among peers. In addition, they must conduct themselves with the highest degree of integrity, professionalism and respect for all members of the workplace.

This program recruits two post-graduate trainees with MD and/or PhD background who will propose research in allergy, asthma or immunology that includes investigation in human subjects or samples. Bench/animal-oriented research proposals should have a translational component, utilizing human subjects or human samples.

Important criteria for applicants:

• Applicants should have a research project with a translational component and a primary mentor.  The projects usually involve a bench research mentor and a clinical research mentor though other arrangements are possible. The main mentor, who will work most closely with the applicant, must be a NUAIR T32 preceptor.  If a potential candidate has identified a mentor that qualifies to serve on NUAIR based on their NIH funding, mentoring success, and relevance to the Allergy-Immunology goals of NUAIR, we are happy to consider adding the mentor/applicant pair to the NUAIR team.
• NIH T32 requires that the individual to be trained must be a citizen or a noncitizen national of the United States or have been lawfully admitted for permanent residence by the training appointment date.
• NRSA Support: No individual trainee may receive more than five years of aggregate Kirschstein-NRSA support at the predoctoral level and three years of aggregate Kirschstein-NRSA support at the postdoctoral level, including any combination of support from Kirschstein-NRSA institutional research training grants and individual fellowships.

For more information on NRSA eligibility requirements, see the NIH Grants Policy Statement on Kirschstein NRSAs.

• A two-year commitment is required, or an earlier departure will incur NIH-payback of the first year of support. 
• Candidate must dedicate at least 75 percent of effort to research during T32 support.
• Candidate must have a strong commitment to a research career.
• Appointment is renewed yearly, and depending on adequate performance. 
• In the initial phase of application, the candidate must submit a resume and an abstract of the research proposal and must indicate the mentors and who will be the main T32 mentor/preceptor in our online portal. Email us at allergy-administration@northwestern.edu ith any questions regarding this process.

Any NRSA postdoctoral trainees or fellow incurs a payback obligation during their first year of support.  Pre-doctoral NRSA trainees do not incur a payback obligation. Payback means that you will perform qualified research or teaching activities for a length of time equal to the period of NRSA support you received. Receiving 12 months of postdoctoral training support obligates you to perform 12 months of qualified research or teaching activities as payback. Only the first year of training incurs a payback obligation; the second year of training pays back the first year, with each month of qualifying payback activity paying back one month of NRSA support. If you receive two full years of NRSA training, you will have completed your payback obligation. In general, payback activity must involve at least 20 hours per week and be conducted over 12 consecutive months. Special exceptions to these requirements may be considered on a case-by-case basis.

Additional resources on Payback Obligations can be found on the NIH website:

• NIH Grants Policy Statement on Payback Requirements
• Payback FAQ
• Payback Activities Certification Form

The Berin Lab aims to improve the prevention and treatment of food allergies by understanding how allergies and tolerance to foods develop. We study immune responses during food allergy clinical trials to identify what drives treatment-based tolerance and to develop better therapies. Our research focuses on T cells, which play a key role in antibody responses and inflammation. Targeting T-cell products is now central to several clinical trials.

We also study Food Protein-Induced Enterocolitis Syndrome, a non-IgE-mediated food allergy linked to innate immune activation, to understand how the immune system recognizes food in these cases.

Since food allergies often develop in the first year of life and can occur the first time a child eats a food, we are investigating factors that trigger early onset. For later-onset cases, we study what causes a breakdown in tolerance to foods that were previously safe.

For lab information and more, view Cecilia Berin, PhD's faculty profile.

Publications

See Berin's publications on PubMed.

Contact

Email Berin

The Eisenbarth-Williams lab focuses on defining the cellular and molecular mechanisms that regulate antibody responses. The development of these antibodies relies on the interactions between three immune cells: dendritic cells (DCs), T cells and B cells. We study how these three cell types communicate to shape different types of antibody responses, some protective in the case of vaccination and some harmful in the case of allergy and alloimmunization. By utilizing human samples to guide our studies and mouse models to test new mechanistic paradigms, we have identified novel and unexpected cell subsets and functions. The fundamental principles governing the interaction between DCs, T cells and B cells are the same across these seemingly disparate responses, yet specialization in the subset of each cell type, the specific niche for the interaction and the cellular signals exchanged between the cells dictates what type of antibody response is generated. This knowledge can be harnessed to induce protective immune responses and subvert pathogenic ones. Our recent work has also led us to focus on how the epithelium of the gut and lung regulate these responses, in particular to food allergens and aeroallergens.

Visit the Eisenbarth-Williams Laboratory website

The Kato Lab studies type 2 inflammation in airway diseases, using chronic rhinosinusitis with nasal polyps (CRSwNP) as a model. CRSwNP, a severe form of chronic rhinosinusitis, is characterized by eosinophilic inflammation and elevated type 2 cytokines like IL-5 and IL-13, but its underlying mechanisms are still unclear.

Our research focuses on thymic stromal lymphopoietin (TSLP), an IL-7-like cytokine that regulates type 2 inflammation. We found TSLP is highly upregulated in nasal polyps and induces inflammation through dendritic cells, Th2 cells, group 2 innate lymphoid cells, and mast cells — all of which are elevated in nasal polyps. We're investigating how TSLP amplifies type 2 inflammation through these cell types.

We also study non-polypoid CRS (CRSsNP), which shows more heterogeneous inflammation. This variability may explain inconsistent findings in CRSsNP studies. Our lab is currently exploring how different inflammatory patterns in CRSsNP affect clinical outcomes.

Publications

See Atsushi Kato, PhD's publications in PubMed.

For more information, view Kato's faculty profile.

The Kuang Lab studies the role of eosinophils and lymphocytes in eosinophilic gastrointestinal diseases (EGIDs) and other eosinophilic disorders like drug-induced eosinophilia, DRESS and hypereosinophilic syndromes. We create well-characterized patient cohorts, collecting clinical data and biological samples to explore these diseases.

EGIDs are chronic, food-triggered disorders that significantly impact quality of life and, if untreated, can cause scarring in the GI tract. Despite the known involvement of eosinophils and T cells in EGID, many questions remain about their roles. Our lab aims to define:

1. Unique blood eosinophil signatures that distinguish EGIDs from other eosinophil-related and atopic disorders.
2. Specialized Th2 cells in EGIDs compared to those in food allergy.

These findings could lead to non-invasive diagnostic biomarkers for EGIDs and reshape our understanding of disease mechanisms in other eosinophilic and food-related conditions.

See Fei Li Kuang, MD, PhD's publications in PubMed.

For more information, visit Kuang's faculty profile.

Contact

Email Kuang

Our lab studies how Siglec family receptors regulate immune cell survival and function. These receptors bind to sialic acid-containing glycan ligands and use inhibitory signaling to suppress inflammation. Each Siglec receptor is expressed on specific immune cells, making them promising therapeutic targets to control inflammatory responses. We focus on Siglec-8 (on eosinophils, mast cells and basophils) and Siglec-6 (on mast cells and basophils) as potential targets for treating allergic diseases, chronic urticaria and systemic mastocytosis.

Our research shows that targeting Siglec-8 induces cell death in cytokine-primed eosinophils through CD11b/CD18 integrin and ROS production. We aim to understand why priming is necessary and how Siglec-8 triggers this pathway. For Siglec-6, we’ve demonstrated that engaging this receptor on human mast cells has an inhibitory effect, which can be enhanced by co-engagement with activating receptors, allowing for precise targeting of disease-causing pathways without depleting mast cells.

We use in vitro systems and transgenic mice to explore Siglec receptor function and potential therapeutic applications.

In collaboration with Tom Hope’s lab, we are also investigating how HIV interacts with human mast cells. Our studies show that mast cells can be infected by HIV and produce intact, replication-competent virions. Understanding this viral reservoir could explain chronic low-grade inflammation and premature aging in people living with HIV and help identify strategies to eliminate the HIV reservoir. We use primary human mast cells, cell lines and humanized mice to study the impact of HIV infection on mast cell phenotype, function and survival.

Publications

View Jeremy O'Sullivan, PhD's publications on PubMed.

For more information, visit O'Sullivan's faculty profile.

Contact

Email O'Sullivan

Aspirin Exacerbated Respiratory Disease (AERD) is also referred to as Samter’s Triad. This disease is clinically defined by the presence of chronic rhinosinusitis with nasal polyps, asthma, and an intolerance to medications that inhibit the cyclooxygenase-1 enzyme. When patients with AERD ingest certain non-steroidal anti-inflammatory drugs (NSAIDs) such as Aspirin or Ibuprofen they develop worsening nasal and respiratory symptoms that can be severe. Even in the absence of taking NSAIDs, patients with AERD on average have more severe sinus disease and asthma compared to patients that have either chronic sinus disease or asthma alone.

The Stevens Lab is currently investigating what cellular and molecular mechanisms may be contributing to this enhanced disease phenotype. In particular, the lab is focusing on the role basophils and eosinophils may have in promoting the chronic inflammation observed in the sinuses. Additionally, the lab is also investigating how specific mediators related to the 15-lipoxygenase metabolic pathway may contribute to AERD disease pathogenesis.

Publications

View Stevens Lab publications via PubMed.
For more information, visit Whitney Stevens, MD, PhD's faculty profile.

Contact

Email Stevens