Immunity: New findings in the field of immunity show how cancer cells evade the immune system.

Scientists are increasingly trying to use the body's own immune system to fight cancer.
study, conducted by the University of Bonn and research institutes in Australia and Switzerland, shows that tumor cells are used to evade such attacks.
developed for this work will help to better understand the "race" between immune defence and disease.
results may help improve modern treatments.
results have been published in the journal Immunity.
cancer cells have a completely different appearance, behavior and active genes from healthy human cells.
, it's not without being ignored: the immune system records something's wrong and sends its troops to fight tumors.
, however, the reaction is sometimes too weak to control or even destroy cancer in the long term.
, researchers have been working for years to strengthen the immune system's defense response.
this case, T cells can detect and kill sick or defective cells.
each T cell is specific to a specific characteristic, also known as an antigen.
, for cancer therapy, researchers are looking for T-cells in patients who can detect tumor antigens.
, they can, for example, amplification and re-inject them into the patient.
in this way, they can enhance the patient's immune response to cancer.
limitations: unfortunately, however, many tumors have developed strategies that allow them to evade the immune system.
scientists studied the strengths of these strategies and the strategies they relied on, in this paper they focused more on skin cancer, or melanoma cells.
Focus: 1, different endogenous target antigens used in the comparison of T-cell therapy 2, melanoma immunoesophageal esoteric by the type and level of target antigens determined 3, target melanin antigen-driven diffusion and myelin immersion 4, carcinogenic antigen persistence can save immuno-checkpoint therapy melanoma in several aspects different from healthy cells.
, for example, a variety of different genes are active in them.
these are potential antigens for T cells.
, which is particularly suitable for triggering a strong and long-lasting immune response? To answer this question, the researchers developed a clever way in their experimental model: they attached a marker to genes active in the development of melanoma cells and used them to produce antigens.
, they released a group of T-cells targeting tumor cells, which accurately identified the molecule as a disease marker.
then used the strategy to study how cancer cells respond to the immune system.
based on genes labeled with the label, they found significant differences.
When T cells target genes responsible for typical melanoma characteristics, we observe that cancer cells change their appearance over time and inhibit those genes," explains Dr. Nicole Glodde, a colleague of Effern's.
so that's how they evade the immune system.
, another gene studied in the study is critical to tumor survival.
makes it not so easy to lower and hide.
, we think the gene has the potential to induce very effective T-cell responses," stressed Effern, a research consultant.
Maike, director of the Institute of Experimental Oncology at the University Hospital of Bonn and a member of the Distinguished Immune Sensory Research Group at the University of Bonn, said: "Our work has the potential to clear the way for more effective immunotherapy.
we have developed to better understand the process by which cancer cells are monitored by the immune system.
study was partly funded by the German Research Foundation (DFG) within the framework of the International Graduate School.
this is why Dr Maike Effern worked for a year at the Peter Doherty Institute in Melbourne, Australia, under the leadership of Professor Thomas Gebhardt, an internationally renowned expert in the field of immunometrics.
The Graduate School between the University of Bonn and the University of Melbourne is an outstanding example of international research collaboration, and for me personally, this experience will have a lasting impact on my future career."
immune escape limits the long-lasting response to T-cell therapy.
here, the researchers examined how the regulation and function of gene products that provide CD8-T cell anti-tumor immune target targets affect therapeutic efficacy and resistance.
they used CRISPR-Cas9-based methods (CRISPitope) in the same melanoma model to fuse cd8 plus T cell epitopes of the same model into the C endos ends of different endogen gene products.
A variety of genetic and non-genetic immune escape mechanisms were revealed through the same table-specific CD8 plus T cell transfer (ACT) targeting melanin proteins or cancer-causing CDK4 R24C (cell cycle protein-dependent kinase 4).
ACT targets melanin proteins, but not CDK4 R24C, which promotes melanoma dedifferentiation and increases myelin cell immersion.
persistence of CDK4 R24C antigens is associated with high interferon and T-cell-rich tumor microenvironments, which can be used as immunotherapy to suppress immunoassociative checkpoints.
, the choice of target antigens determines the esotoplasm and immune status of relapsed melanoma, which is related to the design of cancer immunotherapy.
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