Burkitt lymphoma (BL) is an aggressive non‐Hodgkin lymphoma. The prevalence of BL is ten‐fold higher in areas with stable transmission of Plasmodium falciparum malaria, where it is the most common childhood cancer, and is referred to as endemic BL (eBL). In addition to its association with exposure to P. falciparum infection, eBL is strongly associated with Epstein–Barr virus (EBV) infection (>90%). This is in contrast to BL as it occurs outside P. falciparum‐endemic areas (sporadic BL), where only a minority of the tumours are EBV‐positive. Although the striking geographical overlap in the distribution of eBL and P. falciparum was noted shortly after the first detailed description of eBL in 1958, the molecular details of the interaction between malaria and eBL remain unresolved. It is furthermore unexplained why exposure to P. falciparum appears to be essentially a prerequisite to the development of eBL, whereas other types of malaria parasites that infect humans have no impact. In this brief review, we summarize how malaria exposure may precipitate the malignant transformation of a B‐cell clone that leads to eBL, and propose an explanation for why P. falciparum uniquely has this capacity.

Naturally acquired protective immunity to Plasmodium falciparum malaria is mainly antibody-mediated. However, other cells of the innate and adaptive immune system also play important roles. These include so-called unconventional T cells, which express a γδ T-cell receptor (TCR) rather than the αβ TCR expressed by the majority of T cells—the conventional T cells. The γδ T-cell compartment can be divided into distinct subsets. One expresses a TCR involving Vγ9 and Vδ2, while another major subset uses instead a TCR composed of Vδ1 paired with one of several types of γ chains. The former of these subsets uses a largely semi-invariant TCR repertoire and responds in an innate-like fashion to pyrophosphate antigens generated by various stressed host cells and infectious pathogens, including P. falciparum . In this short review, we focus instead on the Vδ1 subset, which appears to have a more adaptive immunobiology, but which has been much less studied in general and in malaria in particular. We discuss the evidence that Vδ1 + cells do indeed play a role in malaria and speculate on the function and specificity of this cell type, which is increasingly attracting the attention of immunologists.