Kelly Brown

Associate Professor

Research Classification

Research Interests

childhood rheumatic diseases

Relevant Thesis-Based Degree Programs

Affiliations to Research Centres, Institutes & Clusters

Research Options

I am available and interested in collaborations (e.g. clusters, grants).
I am interested in and conduct interdisciplinary research.


In Canada, rheumatic conditions are the most common chronic illness of childhood, affecting as many as 10 000 of our children and youth. Examples of rheumatic diseases are juvenile idiopathic arthritis, lupus, vasculitis and autoinflammatory conditions. The common denominator for all is pain and / or inflammation in joints, muscles, and critical organs. Some diseases are life- or organ- threatening and all have significant potential for lifelong poor health and disability. There are no cures and remarkably few treatments that are specific and safe for a growing child. My research program is designed to generate an evidence base for clinical decisions that ultimately improve outcomes for Canadian children and families affected by rheumatic disease.

Research Methodology

Flow cytometry, ELISA, qPCR, Immunoblotting, cell culture, R statistical language, biostatistical modeling


Postdoctoral Fellows

We are a highly collaborative, multidisciplinary team of scientists that are motivated to improve diagnosis, treatment and outcomes for children and youth with a rheumatic disease through the discovery of driving mechanisms and prognostic biomarkers. Priority rheumatic diseases are: vasculitis - which develops when blood vessels carring oxygen to critical organs in the body (inclusive of the brain, kidneys and lungs) are damaged by inflammation, and systemic autoinflammatory diseases (SAID) - which are caused by unprovoked, recurrent and uncontrolled attacks of inflammation and fever. Specifically, trainees work towards the i) validation and prospective testing of biomarkers for diagnosis and assessment of overall and organ-specific disease activity, and ii) unravel the contribution of innate and adaptive processes to disease onset, severity, and response to treatment.

Ideal team members are basic scientists (BSc, MSc, PhD) that are passionate about improving child health through a translational, 'team science' approach. They may have foundational training in a variety of scientific disciplines (immunology, biochemistry, genetics, computing science). Individuals should be highly motivated and have prior research experience. Strong interpersonal skills and the ability to communicate with scientists, clinicians and patients/families is essential.

All researchers based at the BC Children's Hospital require a Criminal Record Check (CRC) and must provide proof of full vaccination against COVID-19. We encourage applications from members of groups that have been marginalized on any grounds enumerated under the B.C. Human Rights Code, including sex, sexual orientation, gender identity or expression, racialization, disability, political belief, religion, marital or family status, age, and/or status as a First Nation, Metis, Inuit, or Indigenous person. 


I support public scholarship, e.g. through the Public Scholars Initiative, and am available to supervise students and Postdocs interested in collaborating with external partners as part of their research.
I support experiential learning experiences, such as internships and work placements, for my graduate students and Postdocs.
I am open to hosting Visiting International Research Students (non-degree, up to 12 months).
I am interested in supervising students to conduct interdisciplinary research.

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Graduate Student Supervision

Doctoral Student Supervision

Dissertations completed in 2010 or later are listed below. Please note that there is a 6-12 month delay to add the latest dissertations.

Assessment of biological markers to aid subtype classification in pediatric primary systemic vasculitis (2023)

Chronic primary systemic vasculitis (PSV) describes a diverse group of debilitating and potentially life-threatening diseases, characterized by inflammation of blood vessels within various organs such as the kidneys, lungs, brain, eyes, and skin. Subtypes of the small- to medium-sized vessel vasculitides are particularly challenging to classify due to many overlapping clinical symptoms. Their differentiation is important, however, as there is evidence that different subtypes benefit from different treatment approaches. The rarity of vasculitis in children has limited pediatric-specific PSV studies and the clinical approach to pediatric PSV is adapted primarily from adult studies. Not surprisingly, adult-derived classification criteria are imperfect for children and consequently, fail to classify up to two thirds of children with small- to medium-vessel PSV. The objective of this dissertation is to identify genetic markers and select, circulating biomarkers to better our understanding and clinical approach to managing the disease and to improve outcomes of children with chronic PSV. Using biological samples and clinical metadata from a worldwide cohort of children with chronic PSV, this dissertation reports (1) genetic associations specific to pediatric autoimmune vasculitis through employing a genome-wide association study; (2) a high prevalence of autoantibodies to lysosome associated membrane protein-2 in pediatric PSV that correlate to vasculitis-associated kidney dysfunction; and (3) the identification of nine patients, originally diagnosed with chronic PSV, harbouring novel and/or rare variants in adenosine deaminase 2 (ADA2) – these genetic data alongside having abrogated ADA2 enzyme activity have led to their reclassification as having a new monogenic form of vasculitis, deficiency of adenosine deaminase 2. This dissertation reports the first large-scale genotype and biomarker study of primary vasculitis focusing solely on pediatric cases. Improved classification is critical for timely therapeutic intervention, for identification of appropriately classified children for clinical trials, and for research, all of which will improve our understanding of the disease and the quality of life of children suffering from chronic PSV.

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Hyaluronan-mediated modulation of human neutrophil function (2023)

Hyaluronan (HA) is a glycosaminoglycan that in its natural, high molecular mass (HMM) form, promotes tissue repair and homeostasis. With inflammation, enhanced HA metabolism results in HMM HA fragmentation to low molecular mass (LMM) fragments that may act as a damage-associated molecular pattern to initiate innate immune responses. However, the responsiveness of myeloid cells to HA is controversial and largely unknown for neutrophils. Here, I investigated if and how HA can directly affect key immune functions of neutrophils and potentially contribute to the dysregulated neutrophil activation observed in childhood-onset rheumatic diseases. For this investigation, peripheral blood cells from healthy donors were incubated ex vivo with pharmaceutical grade HA of different molecular mass (HMM, LMM and HA fragments
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Master's Student Supervision

Theses completed in 2010 or later are listed below. Please note that there is a 6-12 month delay to add the latest theses.

Platelet factor 4 (PF4), a potential biomarker for disease activity in juvenile idiopathic arthritis (JIA) (2022)

Juvenile idiopathic arthritis (JIA) is the most common cause of youth disability in Canada, characterized by chronic joint inflammation and bone degradation. Common JIA treatment regimens include nonsteroidal anti-inflammatory drugs (NSAIDs), and disease-modifying agents. Currently, there are no reliable means to identify those children with JIA at risk of a more severe or progressive or frequently relapsing disease. Platelets are blood cells with well characterized roles in hemostasis and increasingly recognized contributions to inflammation in chronic inflammatory disease. Specifically, the presence of platelet factor 4 (the most abundant platelet-derived chemokine) and activated platelets have been associated with inflammation in rheumatoid joints in adults. However, the role of platelet-derived proteins in juvenile arthritis has not yet been evaluated. This patient-based study evaluated platelet factor 4 (PF4) as a potential subclinical marker of disease activity in JIA and explored a possible cross-talk with neutrophils and neutrophil-derived S100A proteins (S100A8/9 and S100A12) that have been shown to track with JIA disease activity. Results demonstrated that intracellular (within platelets) and extracellular (in plasma) PF4 was significantly more abundant in healthy children compared to adults, and release of PF4 from thrombin receptor-activated platelets was enhanced with prior exposure to S100A12 and S100A8/9. In contrast, PF4 did not stimulate pro-inflammatory responses (release of reactive oxygen species or S100A protein) by neutrophils. Early in JIA disease course and in the absence of NSAID treatment, there was a moderate correlation between circulating concentrations of PF4 and both disease activity and concentrations of S100A12. For patients in remission, circulating PF4 concentrations were higher in children who relapsed, correlated with the time to first flare, and had a similar probability of predicting a flare compared to S100A12. Overall, this study helped to advance our understanding of the role of platelets in chronic inflammation and provided preliminary evidence for PF4 as a subclinical marker for JIA disease activity.

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