# IL-34 regulation of cutaneous immunity by polarizing myeloid cell differentiation

> **NIH NIH K01** · UNIVERSITY OF CALIFORNIA LOS ANGELES · 2020 · $141,561

## Abstract

PROJECT SUMMARY/ABSTRACT
This proposal describes a five-year mentored training program for the career development of a translational
scientist to examine the mechanism by which a cutaneous pathogen, mycobacterium leprae (mLEP), causes
the expansion of immunosuppressive myeloid derived suppressor cells (MDSC) and M2 macrophages (M)
that produce interleukin (IL)-10, a factor critical for failure of host defense and pathogen persistence in
lepromatous leprosy (L-lep) patients. We will compare the MDSC from L-lep patients with the similar cells seen
in the self-limiting or tuberculoid (T-lep) form of disease. We have identified IL-34 as a potential factor that
leads to the production of the immunosuppressive myeloid cells. This project addresses several goals of
NIAMS using leprosy as a translational model to study mechanisms that impact cutaneous immunity, including:
1) identifying how induction of IL-34 can lead to the production of immunosuppressive myeloid populations
(MDSC and M2 M) that contribute to immune tolerance during cutaneous infection and 2) evaluating how
MDSC and M2 M affect immune responses in leprosy (eg. T cell responses). I completed a PhD investigating
the generation of innate immune responses to self-RNAs associated with lupus autoantigens, and have
completed two postdoctoral fellowships. My first fellowship examined the importance of myeloid cell
development and type I interferon responses in murine sepsis. My second fellowship studied the contribution of
type I interferon to IL-10 production in leprosy. Through this proposal, I will develop new molecular techniques,
including high throughput RNA sequencing with the computational analytical skills required to understand
transcriptional regulation, as well as confocal microscopy. I will also expand my clinical translational skills, by
performing experiments involving skin from healthy controls and leprosy patients, by regular meetings with
clinicians and coursework in translational research. These new techniques and skills can be applied to virtually
any skin disorder. This critical mentored phase of training will be performed under the mentorship of Robert
Modlin, MD, a pioneer in translational cutaneous immunology research, who has trained a number of
independent investigators. Dr. Modlin will help to guide me through the necessary steps to becoming an
independent researcher. The research proposed herein will improve the understanding of how novel myeloid
cells develop and contribute to cutaneous immune tolerance to infection. This program will allow me to develop
all of the skills and tools needed to embark upon this research project as well as future research projects, with
the guidance of a successful mentor capable of assisting me into becoming a successful independent
investigator.

## Key facts

- **NIH application ID:** 9965748
- **Project number:** 5K01AR070911-04
- **Recipient organization:** UNIVERSITY OF CALIFORNIA LOS ANGELES
- **Principal Investigator:** Kindra Kelly-Scumpia
- **Activity code:** K01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $141,561
- **Award type:** 5
- **Project period:** 2017-07-01 → 2021-12-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9965748

## Citation

> US National Institutes of Health, RePORTER application 9965748, IL-34 regulation of cutaneous immunity by polarizing myeloid cell differentiation (5K01AR070911-04). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/9965748. Licensed CC0.

---

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