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Rachel V Stadler

Publications and source records attributed to Rachel V Stadler.

2 recordsLinked to original sources

Malaria and cancer: common features and interactions.

Malaria and cancer are major global health burdens, causing high mortality. While often considered distinct, the two conditions share common features, including continuous cell replication within the body, systemic inflammation, immune modulation and evasion, metabolic reprogramming, endothelial dysfunction, and drug efflux mechanisms. Interestingly, whereas malaria parasite infection promotes Burkitt lymphoma, recent studies in animal models indicate that malaria may activate immune mechanisms against various tumors, thereby improving survival rates. The malaria protein VAR2CSA specifically binds to chondroitin sulfate A in the placenta and metastatic cancer cells, which can be exploited for cancer detection and treatment. Studying the common and unique features of malaria and cancer may facilitate the development of treatment strategies for both diseases.

Humans

Malaria: Factors affecting disease severity, immune evasion mechanisms, and reversal of immune inhibition to enhance vaccine efficacy.

Malaria is a complex parasitic disease caused by species of Plasmodium parasites. Infection with the parasites can lead to a spectrum of symptoms and disease severity, influenced by various parasite, host, and environmental factors. There have been some successes in developing vaccines against the disease recently, but the vaccine efficacies require improvement. Some issues associated with the difficulties in developing a sterile vaccine include high antigenic diversity, switching expression of the immune targets, and inhibition of immune pathways. Current vaccine research focuses on identifying conserved and protective epitopes, developing multivalent vaccines (including the whole parasite), and using more powerful adjuvants. However, overcoming the systematic immune inhibition and immune cell dysfunction/exhaustion may be required before high titers of protective antibodies can be achieved. Increased expression of surface molecules such as CD86 and MHC II on antigen-presenting cells and blocking immune checkpoint pathways (interactions of PD-1 and PD-L1; CTLA-4 and CD80) using small molecules could be a promising approach for enhancing vaccine efficacy. This assay reviews the factors affecting the disease severity, the genetics of host-parasite interaction, immune evasion mechanisms, and approaches potentially to improve host immune response for vaccine development.

Humans