Skip to main content
Explore URMC

Anna Bird, M.S.

Photo of Anna Bird

Pre-doctoral student, Immunology Microbiology & Virology (IMV) Ph.D. Program
University of Rochester School of Medicine and Dentistry
LinkedIn Profile

Professional Bio

Human peripheral blood neutrophils stimulated to produce extracellular traps (NETs)

Human peripheral blood neutrophils
stimulated to produce extracellular
traps (NETs).

I am a pre-doctoral student working in the laboratory of Jennifer Anolik, MD. PhD. I was awarded my Masters of Science in 2014 from the University of Rochester and I am currently working toward my PhD in Immunology. My research interests include autoimmunity, cell biology, and translational science. More specifically, my dissertation projects focus on defining the role of neutrophils in adaptive immune dysregulation in systemic lupus erythematosus in both humans and murine models. In 2015, I was awarded the Clinical Translational Science Institute’s Trainee Pilot grant to study the contribution of neutrophils lupus pathogenesis in the bone marrow (cf. project descriptions below).

Award/honors I have received include the NIH T32 training grant, the Randy N. Rosier Award for excellence in public speaking, the American Association of Immunologists (AAI) Trainee Abstract Award, and travel funding for the Children’s Hospital of Philadelphia Translational Research Workshop. I have used my pre-doctoral training to develop a variety of skills, including multicolor flow cytometry, Amnis Image Stream X® imaging cytometry, immunohistochemistry, RNA sequencing, in vitro assay development, microdissection/laser capture microscopy, as well as experience working with various human and murine tissues. I have also gained experience with applied statistics, teaching, and presentation of my research findings at national conferences. As a recipient of the UR CTSI Trainee Pilot Award, I have had an opportunity to develop effective grant writing skills, as well as experience with the IRB and UCAR review processes, research budgeting, and coordination among a team of co-investigators, clinical coordinators, faculty, and technicians who contribute to the success of my UR CTSI pilot project. I had discovered a passion for translational immunology and I plan to continue pursuing my interest in translational science in my postdoctoral work.

Research Overview

Systemic lupus erythematosus (SLE) is a debilitating autoimmune disease that affects around 1:2000 people. Although treatment for SLE has improved in recent decades, a diagnosis of SLE still entails a lifetime of immunosuppressive therapy and elevated risk of early mortality. A better understanding of the mechanisms underlying SLE pathogenesis is necessary for development of more specific and effective therapeutic options for this complex disease. Lupus involves dysregulation of both innate and adaptive immunity, but the central feature of the disease is loss of self-tolerance by B lymphocytes and production of auto-antibodies. This loss of self-tolerance causes ongoing tissue damage and inflammation, affecting a variety of organ systems. My pre-doctoral research includes two main projects: a) defining the role of neutrophils in the development of auto-reactivity in peripheral lymphoid tissues, and b) examining the contribution of neutrophils to lupus pathology in bone marrow. To see the most recently published findings on these projects, see NIH Online Biosketch.

Defining the contribution of neutrophils to loss of self-tolerance in peripheral lymphoid organs

Lupus features chronic inflammation, which promotes ongoing B cell production of auto-antibodies. Neutrophils contribute to inflammation in lupus by producing elevated levels pro-inflammatory cytokines and B cell survival factors, as well as undergoing extracellular trap formation (NETosis), hypothesized to provide a source of self-antigen. Although the neutrophil population in secondary lymphoid organs expands over the course of disease progression in murine lupus, whether neutrophils are contributing directly to adaptive immune dysregulation or play protective role remains an unanswered question. This project addresses this question and defines the mechanisms underlying neutrophil effects on the dysregulated adaptive immune compartment in peripheral lymphoid tissues.

Examining the contribution of neutrophils to lupus pathogenesis in the bone marrow

In 2015, I was awarded the University of Rochester Clinical and Translational Sciences Institute (UR CTSI) Trainee Pilot to study lupus pathogenesis in human and murine bone marrow. The primary goals of this study are a) define the mechanisms underlying elevated type I interferon previously identified in lupus bone marrow by the Anolik Group, and b) examine whether elevated interferon underlies defects in hematopoiesis in lupus. This UR CTSI pilot will build a better understanding of the pathogenesis of lupus in the bone marrow, and will provide critical background knowledge for identification rational therapeutic targets.


Model for how neutrophils contribute to inflammation in lupus bone marrow.

Bone marrow is the source of hematopoietic cells in adults, but in lupus marrow production of several different leukocyte subsets is dysregulated. The bone marrow of lupus patients is a common site of tissue necrosis, thinning of the bones (osteoporosis), and inadequate leukocyte production, contributing to leukopenia. The mechanisms underlying these defects are not clear, but a growing body of literature suggests marrow defects have significant effects on systemic lupus pathogenesis. Published data from the Anolik lab (Palanichamy et al. 2014) has shown evidence that B lymphocyte development is altered in lupus, possibly driven by an abnormal cytokine milieu in the marrow, including elevated type I interferon signaling and B cell survival factors. I am using the Clinical Translational Science Institute’s Trainee Pilot Award as an opportunity to further elucidate the nature of hematopoiesis defects as well as the mechanisms underlying the abnormal cytokine milieu and elevated cell death in lupus marrow. This project also examines the factors driving chronically elevated type I interferon (IFN) as well as assessing the contribution of granulocytes to IFNα production.

This project examines the role of type I (IFN) as a mediator of pathology in lupus BM and will provide a more complete understanding of lupus pathogenesis, building toward more specific, successful clinical treatments for marrow pathologies, including inadequate hematopoiesis. The findings of this project will not only have implications for lupus, but also shed light on other autoimmune diseases such as rheumatoid arthritis, auto-immune vasculitis, and psoriasis, where neutrophils and type I IFN play related roles in disease pathogenesis. (1)


Palanichamy A, Bauer JW, Yalavarthi S, Meednu N, Barnard J, Owen T, Cistrone C, Bird A, Rabinovich A, Nevarez S, Knight JS, Dedrick R, Rosenberg A, Wei C, Rangel-Moreno J, Liesveld J, Sanz I, Baechler E, Kaplan MJ, Anolik JH. Neutrophil-mediated IFN activation in the bone marrow alters B cell development in human and murine systemic lupus erythematosus. J Immunol. 2014;192(3):906-18. doi: 10.4049/jimmunol.1302112. PubMed PMID: 24379124; PubMed Central PMCID: PMC3907774.

Bird AK, Meednu N, Anolik JH. New insights into B cell biology in systemic lupus erythematosus and Sjogren's syndrome. Current opinion in rheumatology. 2015;27(5):461-7. doi: 10.1097/BOR.0000000000000201. PubMed PMID: 26164595; PubMed Central PMCID: PMC4554755.

To see the most recently published findings on these projects, see NIH Online Biosketch.