A new therapy transforms the immune system against lymphoma

A new therapy transforms the immune system against lymphoma, modern science to it’s best!

Non-Hodgkin Lymphoma (NHL) is a group of lymph node cancer that affects white immune system blood cells known as B cells. B cells in NHL grow out of control in the lymph nodes, spleen, or other tissues, resulting in tumors. In 2020, about 80 000 people will receive a diagnosis of NHL, and 20 000 people will die of NHL, according to the American Cancer Society.

A new therapy transforms the immune system against lymphoma

In cancer patients, immunotherapy is currently one of the most promising treatments. Immunotherapy is intended to “shut down” the immune system of the patient to attack and eliminate a tumor, as opposed to radio or chemotherapy. However, tumors, including NHL, often mutate to become invisible to the immune system, or even exploit immune-cell interactions.

One of the mechanisms used by NHL to disrupt the immune system has now been identified by a team of researchers led by Elisa Oricchio at EPFL. The scientists found that some NHL patients have an over-activated, mutated form of a protein known as cathepsin S. This protein is responsible for cutting other proteins to the surface of the tumor cells into small fragments. These fragments are the mediator of cancer / immune cell communications.

The study’s leading author Elie Dheilly explains that “When cathepsin S is active, cancer cells will interact with immune cells called CD4 + T cells which help the tumor to grow while maintaining the social distance with CD8 + T cells that would attack and kill the tumor.

Identifying this duplicate relationship between cancer cells and t-cells led researchers to genetically eliminate the effect of cathepsin S.

By inverting communication with the T cells, cathepsin S inhibits reduced tumor growth: now, the tumor was assailed by CD8 + T cells, and CD4 + T cells were kept low. This happens when a population of fragments is inducted into something known as “antigen diversification,” which helps the T cells to recognize and kill tumor cells.

Elisa Oricchio states, “We believe that cathepsin S can serve as a major therapeutical target. “Inducing diversification of antigen is an attractive treatment strategy for increasing immunogenicity of the tumor and improving reactions in Lymphoma but also other types of tumors.”

The study included a new imaging technique developed by co-lead author Elena Battistello to measure the activity of Cathepsepsin S specifically. Using this technique, Oricchio and her team identified and developed new inhibitors for the treatment of patients diagnosed with NHL (patent request filed).

A new therapy transforms the immune system against lymphoma

Original article: Eurekalert

The lab of Professor Oricchio is part of EPFL’s School of Life Sciences, a Swiss Institute for Experimental Cancer Research (ISREC). SCCL, the multidisciplinary alliance pursuing essential, translational, and clinical cancer research, is part of the Swiss Cancer Center Léman (SCCL). SCCL’s founding members are the University Hospital in Lausanne (CHUV), the University of Hospital in Geneva (HUG), Lausanne University (UNIL), and Geneva University (UNIGE) and the EPFL.

Other contributors

Swiss Cancer Center Leman
University of Lausanne
Swiss Institute of Bioinformatics
Ludwig Institute for Cancer Research
University Hospital of Lausanne
Centre for Lymphoid Cancer, BC Cancer Agency
EPFL Institute of Bioengineering EPFL
Histology Core Facility
Ulm University and Ulm University Medical Center
Princess Margaret Cancer Center

Reference

Elie Dheilly, Elena Battistello, Natalya Katanayeva, Stephanie Sungalee, Justine Michaux, Gerben Duns, Sarah Wehrle, Jessica Sordet-Dessimoz, Marco Mina, Julien Racle, Pedro Farinha, George Coukos, David Gfeller, Anja Mottok, Robert Kridel, Bruno E. Correia, Christian Steidl, Michal Bassani-Sternberg, Giovanni Ciriello, Vincent Zoete, Elisa Oricchio. Cathepsin S regulates antigen processing and T cell activity in Non-Hodgkin Lymphoma. Cancer Cell 23 April 2020. DOI: https://doi.org/10.1016/j.ccell.2020.03.016

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