# Understanding the Interface of Allo and Auto-Immunity: The Impact of Angiotensin II Type 1 Receptor Antibodies in Pediatric Kidney Transplant Recipients

> **NIH NIH K23** · UNIVERSITY OF CALIFORNIA LOS ANGELES · 2021 · $204,876

## Abstract

PROJECT SUMMARY/ABSTRACT
This proposal outlines a 5-year career development plan for Meghan Pearl, MD, an Assistant Professor in the
Division of Pediatric Nephrology at the David Geffen School of Medicine, University of California, Los Angeles
(UCLA). Dr. Pearl recently completed her fellowship in Pediatric Nephrology at UCLA and is highly motivated
to be starting a career in academic medicine. She has recently obtained a Master of Science in Clinical
Research (degree awarded June 2018) which will provide the ideal foundation for her proposed additional
training. She will benefit from the superior mentorship of Elaine F Reed, PhD, a world renowned leader in
Immunogenetics and Transplant Immunology. Under Dr. Reed’s guidance, Dr. Pearl will complete essential
training objectives which will provide the groundwork for success in achieving her long term goal of becoming
an independent clinical investigator. At the core of her training program will be 1) completing essential training
in transplant immunology through formal coursework and laboratory experience, 2) expanding her statistical
skills through intensive training in computational biostatistics, and 3) acquiring advanced expertise in clinical
trial design, conduct, and management. This education plan will result in the acquisition of the necessary skills
to become an independent physician scientist in transplantation and successfully compete for R01 funding.
Dr. Pearl’s training objectives will be seamlessly integrated with her proposed research, which is focused on
the clinical impact and pathophysiology of angiotensin II type 1 receptor antibody (AT1R-Ab) in pediatric kidney
transplant recipients (KTRs). In her pilot study, Dr. Pearl found that the post-transplant development of AT1R-
Ab, an autoantibody, is significantly more prevalent in pediatric vs. adult KTRs and is associated with allograft
loss and decline in renal function in the first 2 years post-transplant1. The overarching goal of this research is
to identify patterns of AT1R-Ab mediated allograft injury in pediatric KTRs in the first 5 years post-transplant.
We hypothesize that AT1R-Ab mediates vascular inflammation in the allograft leading to decline in renal
function and allograft loss in the first 5 years post-transplant. We further hypothesize that AT1R-Ab activates
endothelial cells within the allograft resulting in unique molecular signatures associated with allograft injury and
loss. This study will not only enrich our understanding of AT1R-Ab pathogenesis, but also serve as a model for
the study of non-HLA antibody mediated allograft injury – an area that is currently very poorly understood.
Pediatric KTRs will have the most to benefit from this work given 1) the high frequency of AT1R-Ab in this
population and 2) their vulnerability to immunologic complications as a result of the need for repeated
transplantation over their lifetimes. This study will help determine the utility of AT1R-Ab testing in immunologic
risk stra...

## Key facts

- **NIH application ID:** 10176385
- **Project number:** 5K23AI139335-03
- **Recipient organization:** UNIVERSITY OF CALIFORNIA LOS ANGELES
- **Principal Investigator:** Meghan Haley Pearl
- **Activity code:** K23 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $204,876
- **Award type:** 5
- **Project period:** 2019-07-01 → 2024-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10176385

## Citation

> US National Institutes of Health, RePORTER application 10176385, Understanding the Interface of Allo and Auto-Immunity: The Impact of Angiotensin II Type 1 Receptor Antibodies in Pediatric Kidney Transplant Recipients (5K23AI139335-03). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10176385. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*
