Bio

After I graduated from TUM medical school in 2023, I began clinical training in pediatrics under Prof. Julia Hauer at the Children's Hospital Schwabing, aiming to become a pediatric oncologist.
During my M.D. research training (Dr. med. sci.) at the Institute for Medical Microbiology, Immunology and Hygiene – mentored by Professors Raquel Mejias-Luque, Markus Gerhard, and Dirk H. Busch – I conducted extensive research on antigen-specific CD8+ T cell responses. This experience sparked my passion for translational immunology and the therapeutic potential of T cell-based approaches.
I believe that children should benefit most from innovative therapeutic development and want to contribute by developing new and better cellular immunotherapies for pediatric malignancies. Therefore, I paused my clinical training and joined the Heitzeneder Lab at the Stanford Cancer Institute as a postdoctoral researcher.

Honors & Awards

  • Paper of the Month, German Society for Hygiene and Microbiology (DGHM) (Apr-2023)
  • Johannes B. Ordner Award for outstanding dissertation, Technical University Munich (Oct-2024)
  • Walter-Benjamin-Fellowship, Deutsche Forschungsgemeinschaft (Nov-2024)

Professional Education

  • Dr. med. sci. (M.D.), Technical University Munich, Immunology (2024)
  • Approbation (medical license), Technical University Munich, Medicine (2023)

Stanford Advisors

Contact

  • Academic
    maxkoch@stanford.edu
    University - Scholar Department: Stanford Cancer Institute Core Position: Postdoctoral Scholar

Additional Info

Current Research and Scholarly Interests

Cellular immunotherapies represent a novel class of treatments that harness engineered living immune cells instead of conventional synthetic drugs and have already shown remarkable clinical success. Their applications continue to expand, improving the prognosis for many diseases.

However, for some cancers—particularly certain pediatric malignancies—outcomes remain poor, and effective immunotherapy options are still lacking.
For example, mortality rates for pediatric bone cancer such as Ewing sarcoma have not significantly improved in the past decade. Another case is T-cell acute lymphoblastic leukemia (T-ALL), which has a worse overall prognosis than B-lineage ALL and cannot be treated with current anti-CD19 CAR T-cell therapies.

To address these unmet needs, we aim to develop new cellular immunotherapies for pediatric cancers. Our approach targets both MHC-restricted epitopes and native surface antigens that are broadly expressed by malignant cells but absent from healthy tissues. We employ both T cell receptors (TCRs) and chimeric antigen receptors (CARs) to engage these targets.

To enhance safety and manufacturing precision, we use non-viral gene delivery methods such as orthotopic TCR replacement, enabling physiological receptor expression by inserting transgenes into the endogenous TCR locus. The resulting T cell products are evaluated using a range of in vitro and in vivo models and will be primed for eventual translation into clinical trials.

Lab Affiliations

All Publications

  • EPICYCLE: A confirmatory preclinical study of the anti-rhabdomyosarcoma efficacy of BET bromodomain and cyclin-dependent kinase 9 inhibitors. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie Haller, B., Richter, G. H., Wachtel, M., Schuler, L., Regina, C., Renz, B., Jens, M., Bechtold, I., Gadasheva, Y., Hamed, E., Kisele, S., Knoblauch, M., Koch, M. R., Lupar, D., Nakano, S., Pardon, K., Pärschke, P. J., Winter, C., Tölch, U., Schäfer, B. W., Banito, A., von Lüttichau, I., Hettmer, S. 2025; 192: 118704

    Abstract

    Hypothesis-driven academic research identifies interventions with likely disease-specific effects. Yet, many candidate drugs fail upon further development, emphasizing the need for acquisition of more robust preclinical data. We demonstrate that planning and executing multicentre confirmatory preclinical studies in an academic setting by applying the quality standards of early phase clinical trials is feasible. Randomization, blinding, stratification by sex of and quality control measures were carried out successfully. The primary objective of our specific study - to confirm synergistic effects of BET bromodomain protein 4 (BRD4) and cyclin-dependent kinase 9 (CDK9) inhibitors against PAX3::FOXO1 (P3F)-positive rhabdomyosarcoma (RMS) - was not met. Post-hoc analyses support that single-agent BRD4 inhibition by JQ1 effectively reduced the growth and viability of P3F+ RMS cells ex vivo with adequate on-target activity as evidenced by reduced expression of P3F, MYCN, MYOG, and MYOD. The antiproliferative effects of JQ1 and vincristine were comparable, and there was trend towards reduced and delayed xenograft growth in JQ1-treated mice. Yet, in vivo assays were flawed by lower xenograft penetrance, variable xenograft latency, gastrointestinal toxicity, and inadequate on-target activity of drugs. We conclude that confirmatory preclinical trials allow for robust assessment of the efficacy of candidate interventions and reduce bias in academic research. The study platform established here provides a framework that may be of particular benefit for the development of new drugs for rare cancers.

    View details for DOI 10.1016/j.biopha.2025.118704

    View details for PubMedID 41161003

  • CagA-dependent Hobit+ gastric tissue-resident memory T cells confer full protection from Helicobacter pylori reinfection. Gut Gong, R., Huang, B., Ralser, A., Friedrich, V., Mibus, C., Engelsberger, V., Koch, M. R., Skerhut, M., Giese, T., Andrä, I., Vieth, M., van Gisbergen, K. P., Semper, R. P., Gerhard, M., Mejías-Luque, R. 2025

    Abstract

    Helicobacter pylori infection is the most prevalent bacterial infection worldwide. Attempts to develop a vaccine have not been successful, partly due to the absence of well-defined immune correlates of protection. The inflammatory response to H. pylori infection is characterised by the recruitment of T cells expressing markers of tissue-resident memory T (TRM) cells to the gastric mucosa. However, the function of TRM cells in gastric tissue during H. pylori reinfection remained poorly understood.We aimed to investigate the induction, development and function of gastric TRM cells during primary and secondary H. pylori infection.We characterised gastric H. pylori-specific TRM cells in mice and humans by flow cytometry, immunohistochemistry, immunofluorescence, ChipCytometry staining and single-cell RNA sequencing. The function of gastric TRM cells was established in H. pylori eradication and reinfection experiments as well as by targeted depletion of Hobit+ TRM cells and neutrophils in mice.Expression of the transcription factor Hobit governs the induction and development of gastric TRM cells, which largely depend on the presence of the H. pylori virulence factor Cytotoxin-associated gene A. H. pylori-specific CD4+ and CD8+ TRM cells resided long-term in the stomach and conferred complete protection from reinfection with the help of neutrophils. Gastric CD8+ TRM cells exhibited varying Hobit expression levels and clustered into distinct subgroups based on distinct transcriptomic and cytokine profiles, suggesting functional specialisation.These findings establish gastric TRM cells as bona fide correlates of protection against H. pylori, highlighting their potential for future prophylactic and therapeutic strategies.

    View details for DOI 10.1136/gutjnl-2025-334781

    View details for PubMedID 40473399

  • CagA-specific Gastric CD8+ Tissue-Resident T Cells Control Helicobacter pylori During the Early Infection Phase. Gastroenterology Koch, M. R., Gong, R., Friedrich, V., Engelsberger, V., Kretschmer, L., Wanisch, A., Jarosch, S., Ralser, A., Lugen, B., Quante, M., Vieth, M., Vasapolli, R., Schulz, C., Buchholz, V. R., Busch, D. H., Mejías-Luque, R., Gerhard, M. 2023; 164 (4): 550-566

    Abstract

    Infection with Helicobacter pylori strongly affects global health by causing chronic gastritis, ulcer disease, and gastric cancer. Although extensive research into the strong immune response against this persistently colonizing bacterium exists, the specific role of CD8+ T cells remains elusive.We comprehensively characterize gastric H pylori-specific CD8+ T-cell responses in mice and humans by flow cytometry, RNA-sequencing, immunohistochemistry, and ChipCytometry, applying functional analyses including T-cell depletion, H pylori eradication, and ex vivo restimulation.We define CD8+ T-cell populations bearing a tissue-resident memory (TRM) phenotype, which infiltrate the gastric mucosa shortly after infection and mediate pathogen control by executing antigen-specific effector properties. These induced CD8+ tissue-resident memory T cells (TRM cells) show a skewed T-cell receptor beta chain usage and are mostly specific for cytotoxin-associated gene A, the distinctive oncoprotein injected by H pylori into host cells. As the infection progresses, we observe a loss of the TRM phenotype and replacement of CD8+ by CD4+ T cells, indicating a shift in the immune response during the chronic infection phase.Our results point toward a hitherto unknown role of CD8+ T-cell response in this bacterial infection, which may have important clinical implications for treatment and vaccination strategies against H pylori.

    View details for DOI 10.1053/j.gastro.2022.12.016

    View details for PubMedID 36587707

https://orcid.org/0000-0003-3865-079X