T cells and neurological disorders. Interview with Daniela Latorre.

Since 2025, Daniela Latorre has been a Group Leader at the Institute of Experimental Neurology, San Raffaele Hospital in Milan. Her post is supported by the Giovanni Armenise Harvard Career Development Award. Latorre obtained a PhD in immunology at the “Sapienza” University of Rome and then moved to Switzerland. From 2020 to 2024, she was Group Leader of the Human Neuroimmunology laboratory at the Institute of Microbiology, ETH Zurich.

She has won numerous national and international career research grants and prizes, including the PRIMA starting grant from the Swiss National Foundation, the Pfizer Research Prize 2020, and the ERC Consolidator Grant in 2024.

Your CDA project is called “Dissecting the autoreactive T cell immunity in human inflammatory peripheral neuropathies”. Can you explain more?

I study the autoimmune response in inflammatory neurological disorders of the peripheral nervous system. These are rare, potentially life-threatening conditions that can cause muscle weakness and paralysis, for which no specific treatments are currently available. My research focuses on autoreactive T cells across different disease subtypes, intending to define their presence and targets and unravel theunderlying mechanisms.

In 2024, you published a landmark Nature paper. What was it about?

It has long been recognized that peripheral neuropathies are caused by autoimmunity, but the underlying mechanisms driving these diseases are still not fully understood. In that paper, we uncovered that in patients with the most common variant of Guillain-Barré syndrome (Acute Inflammatory Demyelinating Polyneuropathy – AIDP), pathogenic T cells infiltrate the nerve tissue and target myelin. Hence, we demonstrated for the first time in patients that neuropathies have an autoimmune component mediated by a dysregulated T cell immunity.

What are the challenges of your research?

Although autoreactive immune cells play a key role in disease immunopathogenesis, they are usually extremely rare. Therefore, detecting them in biological samples requires highly sensitive technologies. On the clinical side, no subtype-specific therapies currently exist for inflammatory disorders of the peripheral nervous system. As a result, all patients are treated with the same nonspecific approaches, leading to highly variable treatment responses, most likely reflecting the underlying heterogeneity of disease mechanisms.

So, what is your strategy?

We work with human cells from patients’ samples: blood, cerebrospinal fluid, and, in some cases, even biopsies of the nerve. Over the past years, I have optimized a highly sensitive workflow that overcomes current limitations in detecting rare autoreactive T cells. This approach allows us not only to identify these cells but also to characterize them with high resolution, providing critical insights into their role in disease.

What is the impact of your research on the scientific community and society at large?

By elucidating the immune mechanisms underlying specific disorders, my research contributes to a deeper understanding of biological processes that may also be relevant to other neurological conditions. In the case of inflammatory peripheral neuropathies, one of the main unresolved questions is whether different disease subtypes are driven by distinct immune mechanisms. Additionally, while many autoimmune disorders are linked to preceding infections, the ways in which these infections influence disease onset and progression remain unclear. Inflammatory peripheral neuropathies offer a unique human model to explore this relationship. Our approach bridges basic science and clinical practice, offering the potential to open new avenues for the development of targeted diagnostic tools and more precise and effective therapies.