Abigail Pajulas

PhD Candidate in Microbiology and Immunology

Indiana University - School of Medicine

About me

Hi, I’m Abigail! I am an Immunologist-in-training, Diversity advocate, and a sub-par rock climber. As an Immunology PhD candidate, I utilize mouse models and bioinformatic approaches to define the role of Interleukin-9 in allergic asthma, lung cancer, and urinary tract infections. I actively participate in DEI initiatives with the Society for the Advancement of Chicanos/Latinx and Native Americans in Science chapter at IU. In addition to the problems in my scientific research, I continue to challenge myself with rock climbing problems/routes.

Feel welcomed to connect with me via LinkedIn!

Download my resumé.

Interests

Allergic diseases (Asthma & Atopic Dermatitis)
Lung cancer
Immunology

Education

PhD Candidate in Microbiology and Immunology, Fall 2018 - present

Indiana University - School of Medicine
BSc in Kinesiology-Exercise Science (Honors), Spring 2018

California State University, Northridge

Academic Appointments

Research, Internships, & Fellowships

Ph.D. Student

Indiana University - School of Medicine: Mark Kaplan lab

May 2019 – Present Indianapolis, IN

As a T32 fellow, I have completed several projects within the Kaplan which include but are not limited to studying the role of IL-9 in allergic asthma, lung cancer, and urinary tract infections. I’ve also contributed to several projects and received recognition in the form of publications. In addition to my research, I serve as a board member in IUSM’s Society for the Advancement of Chicanos/Latinx and Native Americans in Science chapter, in addition to a Toastmasters International club.

Research Student Intern

University of Colorado, Denver - Anschutz Medical Campus: Stefan Pukatzki lab

May 2017 – Jun 2017 Denver, Colorado

I participated in a summer research experience as a Graduate Experience for Multicultural Students (GEMS) intern. As an intern for 10-weeks, I participated in academic seminars, professional development workshops, and conducted research in a Dr. Stefan Pukatzki’s lab. My summer project focused on investigating the role of toxin-coregulated pilus on Vibrio cholerae and its effects on type VI secretion system by using killing assays with Escherichia coli.

Undergraduate Research Assistant

California State University, Northridge: Drs. Luciana Lagana, Taeyou Jung, and Sean Murray

May 2016 – May 2018 Northridge, CA

As a Maximizing Access to Research Careers (MARC U*STAR) T34 scholar, I participated in undergraduate research in several labs:

Jung lab research: Analyzed Brain Activity using fNIR During Dual Task Walking in Individuals with Parkinson’s Disease
Lagana lab research: Assessed the impact of anti-bias films on reducing stereotypes and increasing empathy towards discriminated minorities
Murray lab research: Investigated the role of PhaA, PhaB, and PhaC in promoting (p)ppGpp accumulation in Caulobacter crescentus

Publications

Allergic airway recall responses require IL-9 from resident memory CD4+ T cells

Ulrich et al. used an allergen rechallenge mouse model to study the impact of IL-9 producing immune cells on lung inflammation and recall responses. They found that IL-9 primarily came from multifunctional CD4+ T cell resident memory (Trm) populations present in the lungs of mice. These cells secreted IL-9 in an antigen-specific manner and largely depended on IL-33 for IL-9 up-regulation. IL-9+ CD4+ Trm also had a unique transcriptomic and epigenetic profile compared with other T cell populations in the lung.

BENKAMIN ULRICH, RAKSHIN KHARWADKAR, MICHELLE CHU, ABIGAIL PAJULAS, CHARANYA MURALIDHARAN, BYUNGHEE KOH, YONGYAO FU, HONGYU GAO, TRISTAN A. HAYES, HONG-MING ZHOU, NICK P. GOPLEN, ANDREW S. NELSON, YUNLONG LIU, AMELIA K. LINNEMANN, MATTHEW J. TURNER, PAULA LICONA-LIMÓN, RICHARD A. FLAVELL, JIE SUN, MARK KAPLAN

Allergic airway recall responses require IL-9 from resident memory CD4+ T cells

An IL-9–pulmonary macrophage axis defines the allergic lung inflammatory environment

Fu et al. demonstrate that pulmonary macrophages are a major population of immune cells responding to IL-9 produced in mouse models of allergic airway disease. Mice deficient in the IL-9 receptor had impaired expansion of monocyte-derived interstitial macrophages that promoted airway inflammation dependent on arginase expression. IL-9 signaling also promoted macrophage production of the eosinophil-attracting chemokine CCL5, which was elevated in the serum of patients with asthma and correlated with IL-9 levels.

YONGYAO FU, JOCELYN WANG, BAOHUA ZHOU, ABIGAIL PAJULAS, SHONGYU GAOBASKAR RAMDAS, BYUNGHEE KOH, BENJAMIN J. ULRICH, SHUANGSHUANG YANG, REUBEN KAPUR, JEAN-CHRISTOPHE RENAULD, SOPHIE PACZESNY, YUNLONG LIU, ROBERT M. TIGHE, PAULA LICONA-LIMÓN, RICHARD A. FLAVELL, SHOGO TAKATSUKA, DAISUKE KITAMURA, ROBERT S. TEPPER, JIE SUN, MARK H. KAPLAN