<description>&lt;p&gt;This week on Mendelspod, we speak with &lt;strong&gt;Petter Brodin&lt;/strong&gt;, Professor of Pediatric Immunology at the Karolinska Institutet and Director of Systems Immunology at Imperial College London, about his pioneering work in childhood immune development and his new spatial-proteomics investigations into lupus.&lt;/p&gt;&lt;p&gt;Petter shares how a single lecture on natural killer cells pulled him into immunology, and how early twin studies convinced him that “our immune systems are shaped predominantly by non-heritable factors.” That insight drove him to study the earliest stages of immune development—when newborns leave a sterile environment for a microbial world that imprints their immune trajectories for life.&lt;/p&gt;&lt;p&gt;A major theme of the conversation is Petter’s insistence that immune responses cannot be understood by looking at cells one by one. As he puts it: “Cells don’t ever work in isolation, but historically we’ve always been studying them in isolation—and I think that’s fundamentally problematic.”&lt;/p&gt;&lt;p&gt;This systems view is now being partly enabled by Pixelgen’s spatial interactomics. Using their Proximity Network Assay, Petter’s group is finding that lupus B cells don’t just differ in protein expression—they differ in &lt;em&gt;protein distribution&lt;/em&gt;, revealing organization patterns that classical flow cytometry cannot capture.&lt;/p&gt;&lt;p&gt;These spatial signatures may point directly to new, more precise therapies. Petter explains: “If there is a difference in protein–protein interaction or protein distribution that characterizes disease, then surely that indicates a dysregulation—and that is something we can target.” Instead of broad immunosuppression or depleting whole cell populations, future treatments could focus on the exact cell states driving autoimmunity.&lt;/p&gt;&lt;p&gt;Petter ends on an optimistic note: spatial interactomics won’t just help treat autoimmune disease—it may allow us to intervene &lt;em&gt;earlier&lt;/em&gt;, even preventatively, as we learn how early-life immune disturbances set the stage for disease decades later.&lt;/p&gt; &lt;br/&gt;&lt;br/&gt;This is a public episode. If you'd like to discuss this with other subscribers or get access to bonus episodes, visit &lt;a href="https://www.mendelspod.com/subscribe?utm_medium=podcast&amp;#38;utm_campaign=CTA_2"&gt;www.mendelspod.com/subscribe&lt;/a&gt;</description>

Mendelspod Podcast

Theral Timpson

Petter Brodin of Karolinska: How Spatial Interactomics Could Transform Autoimmune Therapy

DEC 4, 202521 MIN
Mendelspod Podcast

Petter Brodin of Karolinska: How Spatial Interactomics Could Transform Autoimmune Therapy

DEC 4, 202521 MIN

Description

<p>This week on Mendelspod, we speak with <strong>Petter Brodin</strong>, Professor of Pediatric Immunology at the Karolinska Institutet and Director of Systems Immunology at Imperial College London, about his pioneering work in childhood immune development and his new spatial-proteomics investigations into lupus.</p><p>Petter shares how a single lecture on natural killer cells pulled him into immunology, and how early twin studies convinced him that “our immune systems are shaped predominantly by non-heritable factors.” That insight drove him to study the earliest stages of immune development—when newborns leave a sterile environment for a microbial world that imprints their immune trajectories for life.</p><p>A major theme of the conversation is Petter’s insistence that immune responses cannot be understood by looking at cells one by one. As he puts it: “Cells don’t ever work in isolation, but historically we’ve always been studying them in isolation—and I think that’s fundamentally problematic.”</p><p>This systems view is now being partly enabled by Pixelgen’s spatial interactomics. Using their Proximity Network Assay, Petter’s group is finding that lupus B cells don’t just differ in protein expression—they differ in <em>protein distribution</em>, revealing organization patterns that classical flow cytometry cannot capture.</p><p>These spatial signatures may point directly to new, more precise therapies. Petter explains: “If there is a difference in protein–protein interaction or protein distribution that characterizes disease, then surely that indicates a dysregulation—and that is something we can target.” Instead of broad immunosuppression or depleting whole cell populations, future treatments could focus on the exact cell states driving autoimmunity.</p><p>Petter ends on an optimistic note: spatial interactomics won’t just help treat autoimmune disease—it may allow us to intervene <em>earlier</em>, even preventatively, as we learn how early-life immune disturbances set the stage for disease decades later.</p> <br/><br/>This is a public episode. If you'd like to discuss this with other subscribers or get access to bonus episodes, visit <a href="https://www.mendelspod.com/subscribe?utm_medium=podcast&#38;utm_campaign=CTA_2">www.mendelspod.com/subscribe</a>