Heather Gustafson

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Tomorrow is Rare Disease Day.

My family is a family of zebras. We are thriving because of science, researchers, and clinicians who refused to accept no.

Rare diseases are individually uncommon, but collectively common. They require investment and sustained advocacy
rarediseases.org/driving-poli...

@biorxivpreprint.bsky.social comprehensive cell type-resolved transcriptional screen of human cytokine responses
www.biorxiv.org/content/10.6... @helmholtzmunich.bsky.social

Grateful for the mentors who shaped me and the mentees who let me walk with them through their seasons.

My own path has meant getting lost in science — it’s in my DNA — working into the wee hours, weekends, even holidays (healthy or not, TBD). But that’s not the right path for everyone, and that’s the point. Good mentoring is helping someone find the guide who fits their season, even if it isn’t me.

Life has seasons, and success looks different in each one. For some mentees it’s becoming a parent, for others it’s a path to industry or academia. I’ve been so lucky to have mentors who guided me through my seasons, helping me see my path clearly.

Something really special happened yesterday — I received an Outstanding Mentor Award from some truly incredible mentees. Honestly, I learn more from them than they’ll ever know.

🧬🍽️ Your macrophages may be carrying your mother’s metabolic history!
In our @cp-trendsimmuno.bsky.social article, we discuss how maternal diet programs lifelong immune function.
authors.elsevier.com/sd/article/S...
#ImmuneMemory #Macrophages #MaternalNutrition #DOHaD #EarlyLifeProgramming

These findings suggest that approaches used for HLH may help guide treatment strategies for ICANS, especially when tailored to a patient’s unique immune profile.

Reach out if you are here—we’d love to see you!

Using scRNAseq from pediatric B-ALL patients treated with CAR-T, we found that HLH and ICANS share biological overlap, despite clinical differences. We also show patients can reach similar toxicities through different immune pathways-offering insight into why these events are difficult to predict.

Publication #2390 – “Fraternal but not identical twins: HLH and ICANS look a lot alike”

December 6, 5:30–7:30 PM at OCCC – West Halls B3–B4.

Proud to share new work from our team led by Katie Burleigh, with wonderful collaborators across @seattlechildrens.org, UW, Fred Hutch, and St. Jude.

We are so excited for #ASH25! If you are here, we’d love to connect and talk about our work on ICANS, IEC-HS, and hyperinflammation following cancer therapy.

We also found that patients can develop similar toxicities via different immune pathways, providing insight into why these events are often difficult to predict.

Cancer-induced nerve injury promotes resistance to anti-PD-1 therapy - Nature Perineural invasion and cancer-induced nerve injury of tumour-associated nerves are associated with poor response to anti-PD-1 therapy, which can be reversed by combining anti-PD-1 therapy with a...

'Electron microscopy and electrical conduction analyses reveal that cancer cells degrade the nerve fibre myelin sheets. The injured neurons respond by autonomously initiating IL-6- and type I interferon-mediated inflammation to promote nerve healing and regeneration'
www.nature.com/articles/s41...

We are so proud of Bella for all she accomplished this summer! Her curiosity, hard work, and enthusiasm made a real impact. A huge thank you to Nikhita for her thoughtful and dedicated mentorship- she created a positive and supportive learning experience.

Machine Learning of Serum Cytokine and Chemokine Profiles Can Classify Inflammatory Bowel Disease Beyond Clinical Diagnosis from SMI member Tadakazu Hisamatsu.
www.sciencedirect.com/science/arti...

#SMIMemberPaper

Review @cellcellpress.bsky.social @danielboehmer.bsky.social @lozanzi.bsky.social
Interferons in health and disease
www.cell.com/cell/fulltex...

I am beyond excited and incredibly proud to share that our work is now out in @nature.com This discovery was made possible thanks to the first author Kostas kelepouras, my fantastic lab , and the unique research environment here in Cologne in collaboration with the Hospital bambino Gesu in Rome.

Nociceptor neurons suppress alveolar macrophage-induced Siglec-F+ neutrophil-mediated inflammation to protect against pulmonary fibrosis Sensory innervation impacts several lung diseases, but whether it influences pulmonary fibrosis (PF) is unclear. Hiroki et al. report that depletion of TRPV1+ nociceptors leads to worsening of inflamm...

Our latest work on how nerves safeguard lung fibrosis. Congrats to Dr. Hiroki and collaborators. @cp-immunity.bsky.social @kavithascranton.bsky.social @hotchkissbrain.bsky.social @ucalgary.bsky.social @ucalgarymed.bsky.social @libininstitute.bsky.social

www.cell.com/immunity/abs...

Challenging Traditional ADME Assumptions for Physiologically Based Pharmacokinetic Models for Intravenous Administration of Iron–Carbohydrate Nanomedicines: Potential Utility of Gold Nanoparticle Mode... Intravenous iron–carbohydrate complexes are a class of nanomedicines that are widely used globally to treat iron deficiency and iron deficiency anemia associated with a wide spectrum of disease states...

70+ years of iron infusions—safe enough for pregnant women—and we still don’t fully know how they work. What goes into making a safe, effective formula? As always: macrophages are key! I got to be a small part of this fascinating story—link below: link.springer.com/article/10.1...

New perspectives on our work in CAR-T outcomes for ALL!
Is it the fire (inflammation) or the forest (bone marrow health) that shapes patient responses?

Read the commentary in Transplantation and Cellular Therapy:https://www.astctjournal.org/article/S2666-6367%2825%2901304-1/fulltext

It’s Fri-yay! A great day for science. So lucky to get to work with an amazing team!

1/ 🚨 Hot off the press in Nature Immunology: CD4⁺ T cells can license Kupffer cells to rescue dysfunctional CD8⁺ T cells in the liver. Hepatitis B virus (HBV) infection is just the proving ground—this is a paradigm shift in tissue immunity. www.nature.com/articles/s41... 🧵(1/11)

Hypoxia drives progression of multiple sclerosis by enhancing the inflammasome activation in macrophages with Porphyromonas gingivalis infection - Cell Death Discovery Cell Death Discovery - Hypoxia drives progression of multiple sclerosis by enhancing the inflammasome activation in macrophages with Porphyromonas gingivalis infection

TRIF-mediated HIF-1α regulation exacerbates inflammasome activation under hypoxia in response to periodontitis-related bacterial infections, contributing to the progression of autoimmune diseases
www.nature.com/articles/s41...

Caspase-11 drives macrophage hyperinflammation in models of Polg-related mitochondrial disease - Nature Communications Mitochondrial diseases lead to chronic health impairment, aggravated by infections and other environmental exposures. Here authors show, in a mouse model of polymerase gamma (Polg)-related mitochondri...

Delighted to share our paper describing how type I interferon promotes caspase-11 hyperactivity in models of PolG-related mitochondrial disease. Thanks to all co-authors and the POLG Foundation for for their support. www.nature.com/articles/s41...

7/
Key takeaway: all patients had inflammation post-CAR, but outcomes were shaped by their immune system’s ability to manage it.

We need new strategies to support immune recovery and limit harmful inflammation during CAR T therapy.

More is not always better.

End of thread.

6/
Our model:

Patients with sufficient cell numbers dampen inflammation and do well

Those with just enough cells respond, but develop toxicity

Patients with too few cells fail to respond and have runaway inflammation

5/
We also noticed more severe cytopenias in the dysfunctional and toxic groups.

It appears that when patients have fewer immune cells, they can't buffer or "adsorb" the cytokines generated by therapy.

4/
Yes. Higher cytokine levels correlated with worse survival, even after adjusting for tumor burden.

Inflammation wasn’t just a consequence of disease—it was part of the prognosis.

3/
Patients with toxicity "caught up" to the dysfunctional group by day 7—suggesting that the therapy itself is driving inflammation.

But we also saw high levels of inflammation in patients who responded to CAR T without severe toxicity. Could inflammation be a general predictor of poor outcomes?

2/
So we analyzed cytokine and immune response data from days 1, 3, and 7 after CAR T-cell infusion.

What we found was surprising: all patients were inflamed, regardless of clinical outcome.

In fact, the most inflammation was in dysfunctional patients.