# The role of CXCL10 expressing B cells in skin inflammation

> **NIH NIH R21** · THOMAS JEFFERSON UNIVERSITY · 2024 · $195,000

## Abstract

Inflammatory skin diseases, such as psoriasis and allergic contact dermatitis, affect a large proportion of the
population. B cells that suppress inflammation, termed regulatory B cells (Breg), are key contributors to
homeostasis and to limiting inflammation at many sites, including the skin. IL-10 is an important regulatory
molecule used by Bregs to constrain T cell responses. The mechanisms used by Bregs to interact with their
target T cells have not been defined, and no approaches exist to modulate T cell effector functions in skin and
other sites via targeting of B cell properties. Our preliminary data show that IL-10+ Bregs express CXCL10, ligand
for the chemokine receptor CXCR3. Effector CD4 and CD8 T cells are the main cell types that express CXCR3
and chemotax toward CXCL10. We hypothesize that Bregs produce CXCL10 to ‘lure’ effector/memory T
cells into their vicinity and expose them to IL-10 and potentially other Breg molecules, resulting in
dampened T cell responses and decreased inflammation. Alternatively, CXCL10 expressed by effector B
cells may amplify the immune response through enhanced T cell recruitment and/or augmentation of T cell and
B cell activation by facilitating antigen-specific T-B interactions. To test our hypothesis, we propose two specific
aims: Aim 1 will test the role of B-cell expressed CXCL10 during skin inflammation using a mouse model with
inducible B-cell restricted CXCL10-deficiency. Under Aim 2 we will reveal the (IL-10+ and IL-10–) B cell subsets
that produce CXCL10 during skin inflammation as well as determine the effector and regulatory T cell subsets
attracted to skin B cell CXCL10. The gained knowledge will allow us to refine strategies to modulate cutaneous
T cell responses in inflammation, infection, and cancer through targeting B cell functions.

## Key facts

- **NIH application ID:** 10869695
- **Project number:** 1R21AI182763-01
- **Recipient organization:** THOMAS JEFFERSON UNIVERSITY
- **Principal Investigator:** Gudrun Philomena Debes
- **Activity code:** R21 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $195,000
- **Award type:** 1
- **Project period:** 2024-06-06 → 2026-04-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10869695

## Citation

> US National Institutes of Health, RePORTER application 10869695, The role of CXCL10 expressing B cells in skin inflammation (1R21AI182763-01). Retrieved via AI Analytics 2026-05-25 from https://api.ai-analytics.org/grant/nih/10869695. Licensed CC0.

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