# CD200R signaling in tumor growth, immunity and immunotherapy

> **NIH NIH R01** · OHIO STATE UNIVERSITY · 2020 · $356,850

## Abstract

Tumor-associated inflammation and immune responses are key components in the tumor microenvironment
(TME) that regulates tumor growth and progression. Tumor-associated myeloid cells (TAMCs) are a group of
cells that play not only key roles in inducing tumor-associated inflammation/angiogenesis, but also regulate
tumor-specific T cell responses. Thus, identification and characterization of key pathways that can regulate
TAMCs are of critical importance for developing cancer immunotherapy. Our recent studies suggest that
CD200-CD200 receptor (CD200R) interaction may be important in regulating the TME via affecting TAMCs.
We have recently observed that expression of CD200 in melanoma cells significantly inhibits tumor formation
and lung metastasis in immune-competent mice. Conversely, mice deficient for CD200R exhibits accelerated
growth of CD200-positive tumors. Treatment of mice using an agonistic antibody to CD200R significantly
inhibits tumor foci formation in the lungs, suggesting that enhancing CD200R signaling may inhibit tumor
growth. The overall goal of this proposal is to elucidate the roles of CD200R signaling in modulating tumor
associated inflammation and immunity, and its subsequent contribution to tumor growth and progression. We
will also determine if targeting CD200R results in the immune intervention of tumor growth. To achieve these
goals, we will first evaluate the development and progression of various CD200-positive tumors in two strains
of CD200R-deficient mice. Additionally, we will generate Braf/Pten mice with or without CD200R to evaluate
spontaneous melanoma formation, tumor growth, and metastasis (Aim 1). Then, we will evaluate the impacts
of CD200R signaling in the induction of tumor-specific T cell responses in the TME of CD200-positive tumors
(Aim 2). The establishment of these two steps will pave the way to investigate if targeting CD200R can
modulate the TME and if this approach is feasible for cancer immunotherapy (Aim 3). The information
generated from these studies will not only help advance our understanding of tumor pathogenesis and
immunity, but also provide the rationale for CD200R-targeted immunotherapy of human cancer.

## Key facts

- **NIH application ID:** 9972880
- **Project number:** 5R01CA211014-03
- **Recipient organization:** OHIO STATE UNIVERSITY
- **Principal Investigator:** Xue-Feng Bai
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $356,850
- **Award type:** 5
- **Project period:** 2018-08-01 → 2023-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9972880

## Citation

> US National Institutes of Health, RePORTER application 9972880, CD200R signaling in tumor growth, immunity and immunotherapy (5R01CA211014-03). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/9972880. Licensed CC0.

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