SCIENTISTS SPOTLIGHT

Aakanksha Jain, PhD

University of Washington

Subject: Rheumatoid Arthritis

Study Title: Neuronal regulation of T cell fate in autoimmune arthritis

My name is pronounced: Ah-KANK-sha JAY-n

Award: Arthritis and Related Autoimmune Disease Research Grant

Biography: Dr. Aakanksha Jain is an Assistant Professor at the University of Washington, where she leads a research program at the intersection of immunology and neuroscience. She completed her PhD in Immunology at UT Southwestern Medical Center in the lab of Dr. Chandrashekhar Pasare, where she uncovered how autoreactive T cells instruct myeloid cell activation to trigger sterile inflammation and autoimmune pathology. She then trained as a postdoctoral fellow in Dr. Clifford Woolf’s lab at Boston Children’s Hospital, investigating how immune ligands regulate pain in inflammatory diseases.

The Jain lab focuses on understanding how the nervous system and immune system interact to drive painful inflammatory diseases such as rheumatoid arthritis. By deciphering the cellular and molecular mechanisms underlying neuroimmune crosstalk, her lab aims to identify novel therapeutic targets and develop neuroimmune-based therapies for patients suffering from chronic pain and inflammation.

Research Summary: Rheumatoid arthritis is a disease where the immune system mistakenly attacks the joints. This causes severe pain, swelling, and repeated flare-ups of inflammation. Current treatments can reduce symptoms, but they do not usually stop the disease in the long term. One reason arthritis keeps coming back is that a specific type of immune cell, called resident memory T cells, stays in the joints even after inflammation goes away. These cells can quickly restart inflammation, but we do not yet understand how they form in the joints. Studies in patients show that joints without sensory nerves are protected from arthritis, suggesting that nerves might play a role in promoting joint inflammation. Consistently, our data also shows that a nerve-derived molecule called CGRP is important for generating tissue-resident memory T cells. In this project, we will study whether turning off CGRP-producing nerves early in the disease can stop later flare-ups. Findings from this work may also apply to other autoimmune diseases, such as psoriasis and Sjögren’s disease, and could lead to new ways to treat autoimmune conditions by targeting nerve-immune interactions.

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