# MHC class II presentation of Borrelia burgdorferi and synovial tissue antigens in murine Lyme arthritis

> **NIH NIH R21** · MEDICAL COLLEGE OF WISCONSIN · 2020 · $231,000

## Abstract

SUMMARY OF RESEARCH PROJECT
Infections normally elicit an immune response that is sufficiently robust to enable pathogen killing, while also
regulated to limit excessive inflammation and tissue damage. However, inappropriate regulation following
infection may result in development of chronic inflammation and autoimmunity. This project will help determine
how dysregulated T cell responses to specific Borrelia burgdorferi (Bb) and host antigens influence development
of Lyme arthritis (LA) and Lyme-associated autoimmunity.
Lyme disease, caused by infection with the tick-borne pathogen Bb, is usually effectively treated with antibiotic
therapy. However, some patients may develop post-infectious disease manifestations following treatment with
antibiotics, including post-infectious LA, which may cause long-term or permanent disability. Immune
dysregulation and autoimmunity are possible contributing factors to post-treatment Lyme disease syndromes,
which may last months or years after antibiotic therapy. In post-infectious LA, the inflamed synovial lesion is
characterized by accumulation of inflammatory cellular infiltrate, autoreactive T and B cell responses, and
marked synovial fibroblast proliferation, without any evidence of active infection. These features are similar to
the histologic picture seen in other forms of chronic inflammatory arthritis, such as rheumatoid arthritis (RA), the
prototypic autoimmune joint disease.
The objective of this exploratory R21 proposal is to develop novel immunopeptidomics tools using animal models
to identify candidate Bb and self-antigens and to study the biologically relevant antigen presenting cells that
together are driving CD4+ T cell autoimmunity in LA. Once this work is complete, we will have established a
tractable mouse model of Bb infection-induced autoimmunity, providing the research community resources
necessary to rigorously study the foundational parameters of MHC-II induction of autoimmunity to specific self-
antigens, which lie at the heart of pathogenesis in LA and other autoimmune diseases where infection is a
suspected autoimmune trigger.

## Key facts

- **NIH application ID:** 9874294
- **Project number:** 1R21AI148982-01
- **Recipient organization:** MEDICAL COLLEGE OF WISCONSIN
- **Principal Investigator:** Robert Lochhead
- **Activity code:** R21 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $231,000
- **Award type:** 1
- **Project period:** 2020-01-17 → 2021-12-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9874294

## Citation

> US National Institutes of Health, RePORTER application 9874294, MHC class II presentation of Borrelia burgdorferi and synovial tissue antigens in murine Lyme arthritis (1R21AI148982-01). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/9874294. Licensed CC0.

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