DR Congo starts using the ‘mAb114’ Ebola treatment
Outbreak spreads to Ituri
GOMA, Democratic Republic of Congo, Aug 14, (Agencies): Democratic Republic of Congo has started using the experimental mAb114 Ebola treatment on patients in the east of the country, the health ministry said on Tuesday, the first time it has been deployed against an active outbreak.
The outbreak in eastern Congo’s North Kivu province has now spread to neighbouring Ituri province, where a person who was a confirmed case died after returning home from the flare-up’s epicentre in the North Kivu town of Mangina, the ministry said in a statement.
Five new cases have been confirmed, the statement said, bringing the total number of cases to 57 – 30 confirmed and 27 that are considered probable. Forty-one people are believed to have died in all from the haemorrhagic fever.
The mAb114 treatment was developed in the United States by the National Institutes of Health using the antibodies of the survivor of an Ebola outbreak in the western Congolese city of Kikwit in 1995.
It was 100 percent effective when tested on monkeys.
The ministry said that several other experimental treatments have arrived in the regional hub of Beni and are awaiting approval from an ethics committee, including Remdesivir , Favipiravir and REGN3450, REGN3471 and REGN3479.
The outbreak response is challenged by the presence of several armed groups in the densely populated region close to the Uganda border.
Researchers at the Bloomberg~Kimmel Institute for Cancer Immunotherapy in the Johns Hopkins Kimmel Cancer Center discovered inhibiting a previously known protein could reduce tumor burdens and enhance the effectiveness of immunotherapy treatments.
In order to investigate the role of the Yes-associated protein, or YAP, in T-cells in the cancer setting, scientists used mice genetically engineered to lack YAP in several T-cell populations, including regulatory T-cells, known as Tregs. This was the first time the relationship between YAP and Tregs has been explored.
The study was published in Cancer Discovery on June 15, 2018.
Tregs are important for health, because they prevent autoimmune diseases but can be a major obstacle in the mounting of immune responses to tumors and immunotherapy. YAP can be found in a subset of those regulatory T-cells.
Scientists tested the antitumor effects of YAP inhibitors alone and in combination with immunotherapies. Their encouraging results showed YAP plays a role in the suppression of antitumor immunity by Tregs and demonstrated by turning off YAP’s abilities, tumor killing with less restrained immune cells is possible.
Blocking
Fan Pan, MD, PhD, senior author of the study and associate professor of cancer immunology, said blocking YAP or the signaling pathways under its control boosted the effects of both a tumor vaccine and a checkpoint inhibitor (anti-PD1 antibody) to produce even stronger antitumor activity. He said the approach of therapeutically targeting YAP was effective over a broad scope of cancer types in mice.
Since Tregs are notorious for dampening the effectiveness of tumor-directed immunity in cancer patients, this study’s finding may pave the way for a new and promising strategy to unleash the patient immune response from the stifling grip of suppressor cell control.
While Pan and study authors are optimistic that further work could lead to effective YAP-targeting immunotherapies for cancer, they pointed out therapies aimed at enhancing YAP activity may have potential use for the treatment of autoimmune diseases.
The chronic inflammatory disease systemic lupus erythematosus (known as SLE or lupus), is about nine times more common in women than men, and a University of Houston researcher now has the money to find out why. The National Institutes of Health has awarded Chandra Mohan, Hugh Roy and Lillie Cranz Cullen Endowed Professor of biomedical engineering, $2 million dollars to examine the connection.
Mohan knows just where he’s taking the money – straight to the bank. Bank1, that is, a critical gene in B-Lymphocytes, immune cells which make the antibodies that cause lupus when they misguidedly attack the body’s own cells.
“Bank1 exists in men and women, but in women the consequences are more drastic because the Bank1 gene and female hormones work together on the same pathway and make even higher levels of disease-causing auto antibodies,” said Mohan.
Genetic studies have led to the identification of several genes involved with lupus, but how they operate is still unclear. One of these genes is the Bank1.