AI Article Synopsis
- Chronic infection with Plasmodium falciparum is linked to Burkitt's lymphoma, a B cell cancer, though the specific mechanisms are still unclear.
- Researchers used Plasmodium chabaudi in mice to study how chronic malaria infection affects B cell lymphoma development.
- Infection leads to prolonged germinal center (GC) activation and DNA damage in B cells, promoting mature B cell lymphomas that are dependent on the AID enzyme and associated with chromosome translocations.
Article Abstract
Chronic infection with Plasmodium falciparum was epidemiologically associated with endemic Burkitt's lymphoma, a mature B cell cancer characterized by chromosome translocation between the c-myc oncogene and Igh, over 50 years ago. Whether infection promotes B cell lymphoma, and if so by which mechanism, remains unknown. To investigate the relationship between parasitic disease and lymphomagenesis, we used Plasmodium chabaudi (Pc) to produce chronic malaria infection in mice. Pc induces prolonged expansion of germinal centers (GCs), unique compartments in which B cells undergo rapid clonal expansion and express activation-induced cytidine deaminase (AID), a DNA mutator. GC B cells elicited during Pc infection suffer widespread DNA damage, leading to chromosome translocations. Although infection does not change the overall rate, it modifies lymphomagenesis to favor mature B cell lymphomas that are AID dependent and show chromosome translocations. Thus, malaria infection favors mature B cell cancers by eliciting protracted AID expression in GC B cells. PAPERCLIP.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4538708 | PMC |
| http://dx.doi.org/10.1016/j.cell.2015.07.019 | DOI Listing |
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