New research suggests that dendritic cells produce and release CTLA-4, which typically inhibits anticancer responses.Cancer immunotherapy strategies have made it increasingly evident that the immune system plays an integral role in managing and destroying cancer. Nevertheless, many mechanisms of immune suppression exist that may inhibit antitumor immunity. Recently, strategies that implement antibodies directed against negative immunologic regulators have demonstrated significant success. Cytotoxic T-lymphocyte-associate protein-4 (CTLA-4) was the first immunologic checkpoint to be clinically targeted, by the cancer immunotherapeutic ipilimumab, an FDA-approved drug to treat melanoma. After T-cell activation, CTLA-4 is upregulated on the cell surface where it functions to downregulate T cell function. Ipilimumab binds to CTLA-4 on T cells, which blocks the inhibitory signals and enhances anti-cancer immune responses.
A new cancer immunotherapy approach uses nanoparticles carrying tumor RNA to target dendritic cells, leading to a strong anti-tumor response with antiviral-like features.
Researchers have been trying to develop vaccines to fight cancer for decades now, and it is now known to be more difficult than first thought. Cancer progression is not typically characterized by strong inflammatory signals that are necessary to initiate an immune response. Thus, most cancer vaccine strategies are aimed at directly activating a patient’s immune system. Since dendritic cells are extremely well suited at processing and presenting antigens for T cell activation, immunologists are currently working on developing vaccines that target these specialized antigen-presenting cells. Nanoparticles containing a tumor antigen and a dendritic-cell-targeting antibody have proven to be an effective strategy thus far.
Stanford University scientists have identified a single marker that is only expressed in hematopoietic stem cells of the bone marrow.
Grounded in over a half of a century of research, the study of hematopoietic stem cells (HSCs) is one of the most exciting and rapidly advancing fields in medicine today. HSCs have great potential because of two cardinal properties: multipotency, defined as the ability to differentiate into all blood cell lineages, and long-term self-renewal, defined by the inexhaustible ability to produce daughter cells functionally identical to the parent upon cell division. Thus, HSC transplants have been routinely used to treat patients with malignant and non-malignant disorders of the blood and immune system.
McMaster University researchers discovered how an RNA-binding protein regulates self-renewal capacity of cord blood stem cells.
Human umbilical cord blood was once discarded as medical waste, but is now known to be a rich source of hematopoietic stem cells (HSCs). Cord blood stem cells can be potentially used in the treatment of various diseases of the blood, including cancer and other genetic disorders. However, as with other HSC sources, the total number of functional and engraftable stem cells still remains the limiting variable that strongly impacts transplantation success. Identifying methods for robust expansion of HSCs is necessary to generate an inexhaustible source of stem cells for use in regenerative medicine.
Results of a phase II clinical trial show that the outcomes of end-stage heart failure can be significantly improved using stem cells from a patient’s bone marrow.
Heart failure affects approximately 5 million people in the United States, with almost 500,000 new diagnoses each year. Despite advances in treatment to prevent or minimize cardiovascular disease, the restoration of function to a damaged heart remains a major challenge. Since the heart has limited regenerative capacity, transplants are often necessary for cases of end-stage heart failure. Stem cells have the ability to home to damaged tissue and enhance regeneration and remodeling of scar tissue. Thus, therapies using stem cells may potentially lead to more effective treatments for patients with end-stage heart disease.