Melanoma is the most serious form of skin cancer and more likely to grow and metastasize. It has a high response rate to checkpoint inhibitor therapy compared to other cancers; however, about 60% of patients treated do not respond well or relapse. Immune checkpoints are proteins expressed on T cells and function to ensure self-tolerance, but they are also used by tumor cells to limit anti-tumor immune function.
Scientists at antibody engineering company Xencor in Monrovia, CA have just published a research paper that cites using HemaCare sourced leukopaks in the development of their new antibody platform.
Monoclonal antibody therapy has become central to the treatment of many different diseases, including autoimmune disorders, asthma and cancer. Yet in spite of this success, many disease targets have yet to be effectively addressed. Monoclonal antibodies have trouble binding to antigens that are weakly expressed, which results in a need for higher dosing concentrations. High treatment dosages, in turn, can lead to toxicity effects. Monoclonals are also limited in that they can only block one target at a time, leaving parallel disease pathways open that can lead to treatment resistance.
A recent study looked at how checkpoint inhibitors may impact the success of immunotherapy for cancer treatment.
Immune homeostasis is crucial for human and animal survival. The immune system is equipped with cells and factors that maintain a critical balance of signals that prevent immune dysfunction. Pathways that ensure this balance are immune checkpoints, and these are essential for the self-tolerance that prevents autoimmunity. Immune checkpoint proteins modulate T-cell responses to self-proteins and antigens, including tumor antigens. The proteins are expressed on the surface of cancer and cytotoxic T cells, and cancer cells use these to evade attack by T cells.
Chronic lymphocytic leukemia (CLL) is the most common form of leukemia in adults. It is due to the growth of neoplastic B cells in the bone marrow, blood, and lymphoid tissues. People with relapsed/refractory high-risk CLL do not respond to conventional treatments. A possible valuable strategy to design T-cell−based treatment involves the receptor tyrosine kinase-like orphan receptor 1 (ROR1). ROR1 mRNA is found to be highly expressed in CLL cells; however, it is not found to be expressed in other bone marrow–derived cells, including blood cells, or normal adult non-hematopoietic cells. Higher expression of ROR1 in CLL cells was correlated with lower CLL survival. Therefore, ROR1 may play a key role in the progression of CLL.
Minimal change disease (MCD) is a kidney disease characterized by pathology in the glomeruli. The disease has its name because changes associated with it can only be seen via electron microscopy. The effects on the glomeruli lead to its increase in permeability and subsequent severe loss of proteins in the urine. Immunological changes in the kidney tissue are thought to promote the development of MCD. Research studies have suggested that abnormalities in Foxp3 T regulatory (Treg) cells, which control immune homeostasis, are involved in MCD pathogenesis.
