Researchers at the University of Birmingham have made a discovery in the understanding of how our genetic make-up can impact within the activity of the immune system and our ability to fight cancer.

The study, conducted in conjunction with researchers through Birmingham’s Queen Elizabeth Hospital, was published today within Science Signaling and focusses on a protein called ULBP6.

Proteins comprise of hundreds or thousands of smaller units called proteins, which are attached to one another in long chains. Proteins perform most of the work in cells and are required for the structure, perform, and regulation of the body’s tissues and organs.

Lead author of the study Professor Paul Moss from the University of Birmingham’s Institute of Immunology plus Immunotherapy, said: “We worked on a protein called ULBP6 which leads to the removal of damaged cells and an interesting statement has been that there are two types of this protein found in each person.

“This is important as previous studies have demonstrated that the type of protein that we inherit from our parents may influence our risk of auto-immune disease and have an effect on how we respond to some forms of cancer treatment.

“The ULBP6 protein is found on the surface of damaged tissues, including several types of cancer cells, and acts as a ‘flag’ in order to signal to white cells in our immune system that the broken cell should be killed.

“Interestingly, there are 2 major types of this protein in the population and people who inherit a certain subtype have been shown to have a poor outcome right after stem cell transplantation, a procedure used to treat leukemia, that is commonly referred to as ‘bone marrow treatment’. ”

Professor Ben Willcox, also from the University of Birmingham’s Institute of Immunology and Immunotherapy, said: “The 2 types of ULBP6 differ only by two amino acids away from a total of around 180 and it has surprised us this can have such an important influence on patient outcomes.

“In the study we found that one form of ULBP6 forms a very strong bond indeed with its receptor NKG2D on the immune system.

“In addition, when the proteins is released into the local environment it can act in order to block the signalling pathway.

“The ‘sticky’ form of ULBP6 binds over 10 times more highly to NKG2D but a major surprise was that this served to reduce killing by the immune system rather than increase it.

“We now want to understand how this information might be utilized to improve the outcome of patients undergoing stem cell transplantation. inch

The study was funded by the Bloodwise as well as the Wellcome Trust. Bloodwise, the UK’s specialist blood malignancy charity, funds world-class research and offers expert information plus support to anyone affected by leukemia, lymphoma, myeloma along with other blood cancer related disorders.

Alasdair Rankin, Director of Research at Bloodwise, said: “For some individuals with leukemia and other types of blood cancer, stem cellular transplantation can mean the difference between life and death.

“But a stem cell transplant is a gruelling procedure which sadly does not always work, so we require research to improve success rates.

“This research is not going to change care today, but it helps us understand why transplants work less well in some people, which is an important phase on the path to developing better transplant therapy for more people coping with blood cancer. ”

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