Bio

After I graduated from medical school in 2023, I began clinical training in pediatrics under Julia Hauer at the Children's Hospital Schwabing, aiming to become a pediatric oncologist.
Since I enrolled in the M.D. program (Dr. med. sci.) at the Institute for Medical Microbiology, Immunology and Hygiene lead by Dirk Busch and Markus Gerhard, I have become intrigued by CD8+ T cells and their potential in fighting human disease.
I believe that the focus of most therapeutic development efforts should be on children. Driven by this conviction, I have shifted my research to the field of cellular immunotherapies for malignant pediatric diseases, pausing my pediatric residency to join the Heitzeneder Lab at Stanford 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 are a novel kind of treatment leveraging modified living immune cells instead of synthetic drugs and have delivered impressive outcomes so far. Their successful applications are continuously extended, improving the prognosis of many diseases.
However, for some cancer entities, the outcomes are relatively bad and reliable immunotherapy options are still lacking.
One example is the pediatric bone cancer Ewing sarcoma, which's mortality rates, despite of the intensive application of traditional treatments such as surgery, radiotherapy and chemotherapy, haven't improved in the last decade .
An other example is the T-ALL that has a poorer overall outcome when compared with B-lineage ALL and cannot be tackled by standard of care anti-CD19-CAR T cells.

For these pediatric cancers, I seek to develop new cellular immunotherapy.
We targeting both MHC-restricted epitopes and native antigens generally exposed by the malignant cells and not present by most other healthy tissues. We exploit both TCR and CAR as receptors for the candidate targets. Further, we want to leverage non-viral introduction approach like orthotopic TCR replacement to insert the receptors into the endogenous TCR resulting in physiological expression pattern.
The eventual resulting product will have been tested in extensive in vitro and in vivo orthotopic NSG xenograft models and therefore will be ready for clinical trials.

I am convinced that this work will advance the field of cellular therapies in general and specifically will provide new treatment possibilities for pediatric patients with recurrent and refractory cancers.

Lab Affiliations

All Publications

  • 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