Congratulations to Christoph who received the “Basic Immunology” poster prize at the SSAI meeting in Lugano for research into how rare inherited immune disorders can alter the survival and selection of immune cells.
He presented findings from a collaborative study of five inborn errors of immunity (IEIs): HA20, APLAID, DADA2, IKAROS haploinsufficiency, and autoimmune lymphoproliferative syndrome. Some people with these conditions have an increased risk of developing lymphoma, but the biological processes connecting immune dysfunction and cancer remain incompletely understood.
To investigate this connection, we analyzed the antigen receptor repertoirs of B and T cells and found that the B cell receptor repertoire was particularly affected. Several disorders showed reduced diversity or an unusual expansion of selected B cell populations. Conditions affecting key immune signaling pathways also shared an increase in self-reactive B cell receptors, including receptor patterns previously associated with lymphoma.
These findings suggest that a single inherited change in immune signaling can weaken the checkpoints that would normally remove self-reactive cells. This may allow potentially harmful immune cells to survive, multiply, and under some circumstances progress toward lymphoma.
The work contributes to a better understanding of how single mutations that are not only causing immunodeficiency syndromes but are also found in lymphomas reshape immune-cell populations towards lymphoma-like states.

In a new study published in Communications Medicine, we examined together with a team of national and international collaborators how an experimental immunotherapy may help the immune system recognize adrenal cancer.
The treatment, called EO2401, contains peptides derived from common gut bacteria that resemble proteins found in cancer cells. By combining EO2401 with the checkpoint inhibitor nivolumab, we aimed to activate existing immune memory and direct T cells toward tumor-related targets.
We analyzed blood samples from 11 patients with advanced adrenal tumors before and after treatment. At the start of the study, patients had a particularly limited range of T cells compared with healthy individuals and patients with another cancer type. Treatment did not cause the same individual T cell clones to expand across all patients. Instead, it broadened several pre-existing groups of related T cells, recruiting new members into these immune-cell families.
Many of the observed T cell patterns resembled responses previously associated with viral infections and shared tumor proteins. This supports the idea that microbial mimicry could help mobilize existing immune defenses against cancer.
Because the study involved a small group of patients with a rare cancer and EO2401 was given together with nivolumab, further research is needed to elucidate the peptide vaccine’s specific contribution and determine whether these immune changes translate into lasting clinical benefits. The findings nevertheless provide encouraging support for developing OncoMimic-based immunotherapies for rare and difficult-to-treat cancers. Read here.
Congratulations to Sarah and her colleagues from Karolinska Institute in Stockholm and the Allen Institute for Immunology in Seattle for their new review on how aging reshapes T cells and whether declining immune function can be slowed or reversed, now published in Immunity.
Over a lifetime, the immune system builds a valuable record of previous infections. At the same time, the thymus produces fewer new T cells, reducing the variety of unfamiliar threats the immune system can recognize. The result is an immune system that retains extensive experience but becomes less flexible when facing new infections, cancer, or vaccines.
The article describes how lifelong exposure to viruses, chronic inflammation, and changes in tissues can reshape memory T cells. Within individual cells, shorter telomeres, impaired mitochondria, and lasting changes in gene regulation may further weaken their ability to multiply and respond. However, these effects vary considerably between people, showing that immune aging is not a uniform or inevitable process.
The review also highlights potential rejuvenation strategies. These range from improved vaccine formulations and treatments that support new T cell production to metabolic interventions, anti-inflammatory therapies, and emerging approaches that directly reprogram aging cells. Exercise and dietary interventions may also help preserve immune function. Most targeted treatments remain experimental, and any intervention must avoid disrupting the useful immune memory built over decades.
Rather than simply making the immune system “young” again the goal should be to maintain resilience: preserving protection from past threats while keeping enough flexibility to respond to new ones.