Quirin Hammer

We will be recruiting future colleagues at multiple levels (doctoral students, post-docs, and undergraduates) soon, so if you are excited about our work and would like to join us in Kiel, feel free to get in touch already now

...and everybody who supported me along the way, among others Hans-Gustaf Ljunggren, Karl-Johan Malmberg (@malmberglab.bsky.social), Evren Alici, Chiara Romagnani (@romagnanilab.bsky.social), and many more!

I also look forward to supporting and inspiring the next generation of scientists through teaching and supervision.
I’m incredibly grateful to my team at the Karolinska Institute @ki.se...

This marks not only a personal milestone, but also an exciting opportunity to advance our understanding of how NK cells, ILC, and innate-like T cells contribute to protection against infections and to explore their roles in chronic inflammatory diseases

I’m deeply honored to share that I have been appointed W1 Professor 🎓 at the Faculty of Medicine of Kiel University (@uni-kiel.de) and the University Hospital Schleswig-Holstein (UKSH)

Endurance-trained older adults have NK cells with greater functional adaptability, reduced senescence, and enhanced metabolism under inflammatory and pharmacological stress
www.nature.com/articles/s41...

YouTube video by Quirin Hammer Peptide-specific recognition of viruses and virus strains by NK cells

Missed the talk or couldn’t make it to the conference across the globe? No problem! I recorded a rehearsal version of the presentation (yes, I went over time 😅), and you can watch it on YouTube here: www.youtube.com/watch?v=7dU0...

About a month ago, I had the honor of giving an invited talk at #NK2025 in beautiful Tasmania. It was a real pleasure to connect with so many bright minds in the field and share some of our latest work on #NKcells and #viruses.

Interesting technical report by Carsten Watzl & colleagues in @eurjimmunol.bsky.social
We‘ll be sure to give it a go in our assays

Very excited to present at this upcoming seminar series! I’ll be sharing our latest data and our enthusiasm on #NKcells in #virus infections. Registration is free, looking forward to seeing you online

Granzyme K activates the entire complement cascade | Nature Granzymes are a family of serine proteases that are mainly expressed by CD8+ T cells, natural killer cells and innate-like lymphocytes1. Although their primary function is thought to be the induction of cell death in virally infected cells and tumours, accumulating evidence indicates that some granzymes can elicit inflammation by acting on extracellular substrates1. We previously found that most tissue CD8+ T cells in rheumatoid arthritis synovium, and in inflamed organs for some other diseases, express granzyme K (GZMK)2, a tryptase-like protease with poorly defined function. Here, we show that GZMK can activate the complement cascade by cleaving the C2 and C4 proteins. The nascent C4b and C2b fragments form a C3 convertase that cleaves C3, enabling the assembly of a C5 convertase that cleaves C5. The resulting convertases generate all the effector molecules of the complement cascade: the anaphylatoxins C3a and C5a, the opsonins C4b and C3b, and the membrane attack complex. In rheumat

Granzyme K, a serine protease from immune cells like CD8⁺ T, NK cells, triggers the complement cascade, extending beyond cell death to inflammation pathways. PMID:39914456, Nature 2025, @Nature https://doi.org/10.1038/s41586-025-08713-9 #Medsky #Pharmsky #RNA @geneticssociety @eshg 🧪

An eppendorf centrifuge in that specific nicotine-yellow color from the 80s. It's the exact color as the old fridge in your garage that you keep sodas in that your parents replaced in 1997, and which has outlived a half-dozen of its replacements.

"Why don't you buy a new centrifuge"

Because everyone knows that any appliances in that shade of yellow will outlive you and your entire family, look at it

There are two kinds of people in the world: those who fold the edges of autoclave tape over on itself before sticking, and monsters

It's more of a comment than a question

Antiphospholipid syndrome patients exhibit early IFN-driven B cell abnormalities and T & NK exhaustion that impairs immune surveillance of autoreactive B cells through HLA-E-NKG2A interactions
www.researchsquare.com/article/rs-5...

Role of CLASP1/2 in the maturation of the lytic immune synapse in NK cells with evidence of contribution of Golgi derived microtubules
doi.org/10.1101/2025...

Our new work on optimising CAR-T cell sensitivity is now on bioRxiv!

Optimising CAR-T cell sensitivity by engineering matched extracellular sizes between CAR/antigen and CD2/CD58 adhesion complexes

biorxiv.org/cgi/content/...

Thank you for sharing our work here - still pretty new to Bluesky!

Thanks for sharing our work!

Thanks for highlighting our work!

Friends, it's fun to see the #immunology community continue to grow! I created a 4th Starter Pack to help folks find each other. If you're an immunologist and you don't see yourself on the lists, let me know 🧪

go.bsky.app/PY5tCas

go.bsky.app/FmERUoD

go.bsky.app/6aT6qDS

go.bsky.app/QSEPDoj

Cytomegalovirus (CMV) is the leading cause of infectious birth defects and linked to many other morbidities such as with transplantation. For the first time after >50 years of pursuit, a vaccine is in reach jci.org/articles/vie...

Overcoming CD226-related immune evasion in AML with CD38 CAR-engineered NK cells
www.cell.com/cell-reports...

This is amazing to think about! I would love to browse through a few printed sequences like CAG-GTG-ATT-AAC…oh wait there‘s also an AAT variant here

NK cells restrain cytotoxic CD8+ T cells in the submandibular gland via PD-1–PD-L1 PD-L1–expressing NK cells restrain cytotoxic CD8+ T cells in the SMG, providing insights into disrupted immunoregulation contributing to irAEs.

PD-L1–expressing NK cells restrain cytotoxic CD8+ T cells in the submandibular gland, providing insights into disrupted immunoregulation contributing to immune-related adverse events
www.science.org/doi/10.1126/...
@sciimmunology.bsky.social

Cells

The work was really driven by Eleni, our outstanding research assistant! And we thank all colleagues, collaborators, and funders for their important support. Including @karolinskainst.bsky.social, @vetenskapsradet.bsky.social, and many many more

9/9 In summary, our three studies together underscore the dynamic interplay between NK cells and viruses - using SARS-CoV-2 as a model for a newly emerged virus, we exposed an intriguing NK cell recognition mode and how the virus adapts to it

Fitness effects of mutations to SARS-CoV-2 proteins - PubMed Knowledge of the fitness effects of mutations to SARS-CoV-2 can inform assessment of new variants, design of therapeutics resistant to escape, and understanding of the functions of viral proteins. How...

8/9 Finally, we leveraged the massive database of @nextstrain.org, revealing an association between the pM2I mutation and enhanced virus fitness as estimated across more than 6 million SARS-CoV-2 genomes isolated from patients (for details, see here the amazing paper here: tinyurl.com/yv7phs73)

7/9 …for the NK cells, this means that loss-of-inhibition is reverted and, in turn, inhibition via NKG2A is recovered. As such, the disadvantageous effect of the ancestral peptide is lost, indicating a molecular adaptation of the virus to NK cell recognition