Junko Sawada, DVM, Ph.D.

Research Areas

In many diseases—from autoimmune disorders to cancer—the presence and organization of specialized lymphoid structures can be a critical factor determining outcomes. By directing immune cell behavior, these structures sometimes enhance protective responses, such as anti-tumor immunity, but can also drive harmful, chronic inflammation in autoimmune conditions. Understanding how they form, the stromal cells that build them, and the factors (including sex bias) that influence their function is therefore crucial. Our research seeks to bridge fundamental immunology and clinical application, uncovering strategies to harness or modulate lymphoid structures for improved patient care.

• Lymphoid Structure Development

We explore the formation, organization, and functional dynamics of lymphoid structures, which include both secondary lymphoid organs (such as lymph nodes) and tertiary lymphoid structures (TLSs). TLSs often arise in chronically inflamed tissues, including those found in cancer and autoimmune diseases. Our goal is to uncover the mechanisms that regulate lymphoid structure development and function, focusing on the roles of fibroblastic reticular cells, follicular dendritic cells, and endothelial cells.

• Cancer Research

We investigate how certain patients generate TLSs that strengthen anti-tumor immunity, as well as the role of cancer-associated fibroblasts (CAFs) in shaping the tumor microenvironment. By examining these stromal components—alongside fibroblastic reticular cells, follicular dendritic cells, endothelial cells, and immune cell populations—we aim to uncover mechanisms that can be leveraged to enhance anti-tumor responses and improve therapeutic outcomes.

• Sex Bias in Disease Susceptibility

Many autoimmune disorders, including rheumatoid arthritis, multiple sclerosis, and Sjögren’s syndrome, disproportionately affect women, whereas women are generally less susceptible to numerous cancers. We investigate these disparities by examining incomplete X-chromosome inactivation in the stromal cells that shape lymphoid structures. We also maintain a complementary interest in how TLSs—particularly those supported by specialized fibroblasts and other stromal cells—contribute to chronic inflammation in autoimmune conditions. By integrating these approaches, we aim to uncover factors that drive both autoimmunity and sex-specific disease outcomes.