疟疾,Burkitt淋巴瘤 z-bo 2020-09-19 364

　　The link between malaria and Berkit lymphoma was first explained 50 years ago, but the mechanism by which parasitic infection makes immune cells cancerous remains a mystery. Burgit's lymphoma is a rare type of invasive B-cell lymphoma. Berkit first described this lymphoma in African children in 1958. Similar cases have been found worldwide. This type of lymphoma accounts for 30-50% of childhood lymphoma cases, while this type of adult lymphoma accounts for only 1%. If left untreated, Berkit lymphoma will quickly kill the patient.

　　People who have been infected with a specific pathogen for a long time have an increased risk of developing lymphoma. For example, in equatorial Africa where malaria is endemic, Burkitt’s lymphoma is 10 times more common. It has not been clear how the malaria-causing Plasmodium falciparum promotes canceration of blood cells. David Robbiani of the Rockefeller University and his colleagues have decided to solve this problem by studying malaria infection in mice. They found that in the long-term immune response to malaria, B lymphocytes proliferate in large numbers and express a protein called activation-induced cytidine deaminase (AID) for a long time. Under normal circumstances, AID will mutate antibody gene DNA to promote DNA shuffling and produce various antibodies necessary for fighting infection. However, Robbiani's team found that in B lymphocytes infected with malaria, AID caused extensive and severe damage, rearranging the DNA of other genes, some of which are related to the formation of cancer. done

　　Obbiani said: "AID is an inevitable risk factor. Fighting infection requires AID to produce powerful antibodies, which can cause accompanying damage and cause DNA breaks and mutations, thereby increasing the risk of cancer."

　　Obbiani pointed out that hepatitis C virus and Helicobacter pylori infection, as well as some autoimmune diseases, are also associated with long-term B lymphocyte activation and increased risk of lymphoma. Therefore, some targeted strategies to reduce accidental DNA damage caused by AID can help reduce the risk of lymphoma in patients with these diseases.