Chronic malaria and splenic lymphoma: clues to understanding lymphoma evolution

Bates, Imelda; Bedu-Addo, George

doi:10.1038/sj.leu.2400878

Cited by 33 publications

(19 citation statements)

References 37 publications

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“…A berrant immune activation induced by chronic infections with Plasmodium falciparum leads to polyclonal B cell activation characterized by the presence of hyperglobulinemia (1), elevated titers of autoantibodies (2,3), and frequent occurrence of Burkitt's lymphoma (4) and splenic lymphoma (5). The mechanisms that lead to this polyclonal B cell activation are poorly understood.…”

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confidence: 99%

Increased B Cell Survival and Preferential Activation of the Memory Compartment by a Malaria Polyclonal B Cell Activator

Donati

Mok

Chêne

et al. 2006

The Journal of Immunology

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Chronic malaria infection is characterized by polyclonal B cell activation, hyperglobulinemia, and elevated titers of autoantibodies. We have recently identified the cysteine-rich interdomain region 1α (CIDR1α) of the Plasmodium falciparum erythrocyte membrane protein 1 as a T cell-independent polyclonal B cell activator and Ig binding protein. Here, we show that, although the binding affinity of CIDR1α to human IgM and IgG is relatively low, B cell activation still proceeds. CIDR1α rescues tonsillar B cells from apoptosis, and increases the proportion of cycling cells. Comparison of the impact on naive and memory B cell compartment indicated that CIDR1α preferentially activates memory B lymphocytes. Analysis of the gene expression profiles induced by CIDR1α and anti-Ig activation using a cDNA microarray demonstrated a low degree of homology in the signatures imposed by both stimuli. The microarray data correlate with the functional analysis demonstrating that CIDR1α activates various immunological pathways and protects B cells from apoptosis. Together, the results provide evidence for a role of malaria in preferentially activating the memory B cell compartment. The polyclonal B cell activation and augmented survival induced by CIDR1α is of relevance for understanding the mechanisms behind the increased risk of Burkitt’s lymphoma in malaria endemic areas.

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confidence: 99%

Increased B Cell Survival and Preferential Activation of the Memory Compartment by a Malaria Polyclonal B Cell Activator

Donati

Mok

Chêne

et al. 2006

The Journal of Immunology

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“…The dysregulated immune response to long-term carriage of parasites at low levels likely explains the occurrence of HMS and also promotes the development of complications such as marginal zone splenic lymphoma. 8 Experimental studies have shown evidence that Plasmodium spp. invasion proteins bind to uninfected erythrocytes serving as targets for complement-mediated lysis or macrophage phagocytosis.…”

Section: Discussionmentioning

confidence: 99%

HMS-Related Hemolysis after Acute Attacks of Plasmodium vivax Malaria

Mitjà

Hays²,

Malken³

et al. 2011

The American Society of Tropical Medicine and Hygiene

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Among a cohort of 1,213 cases treated for Plasmodium vivax malaria from an isolated Papua New Guinean population, seven adults with severe and sustained hemolytic anemia after clearance of the peripheral parasitemia were prospectively investigated. All the patients fulfilled the criteria for hyper-reactive malarial splenomegaly and in 2 of 7 cases an IgG warm antibody was identified. Hereditary hemolytic anemia was excluded in 5 of 5 patients. All treated cases improved after an initial high dose of prednisone and antimalarial chemoprophylaxis. The persistence of marked anemia in a patient with splenomegaly after a P. vivax attack should raise the suspicion of hyper-reactive malarial splenomegaly.

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“…In patients from areas of endemicity, a differential diagnosis of malaria from lymphoma becomes a challenge when clinical presentation or potential relapse is accompanied by fever and splenomegaly (2). A few cases of malaria have been reported in patients with diffuse large-B-cell lymphoma (1,15,18), which is often associated with a splenectomy and with febrile neutropenia observed at the time of chemotherapy.…”

Section: Case Reportmentioning

confidence: 99%

Malaria Hidden in a Patient with Diffuse Large-B-Cell Lymphoma and Sickle-Cell Trait

et al. 2011

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We report a case of an African patient with sickle cell trait who was diagnosed in Spain with B-cell lymphoma. Blood smears were negative for malaria, and no plasmodium antigens were detected in the blood. To treat his lymphoma, the patient underwent chemotherapy and autologous stem cell transplantation. Following a splenectomy due to a worsening condition, he developed clinical malaria with detectable parasitemia. This case suggests that the humoral response and parasite removal by the spleen

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Chronic malaria and splenic lymphoma: clues to understanding lymphoma evolution

Cited by 33 publications

References 37 publications

Increased B Cell Survival and Preferential Activation of the Memory Compartment by a Malaria Polyclonal B Cell Activator

Increased B Cell Survival and Preferential Activation of the Memory Compartment by a Malaria Polyclonal B Cell Activator

HMS-Related Hemolysis after Acute Attacks of Plasmodium vivax Malaria

Malaria Hidden in a Patient with Diffuse Large-B-Cell Lymphoma and Sickle-Cell Trait

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