Publications by authors named "Adesola C Olatunde"

Malaria comprises a spectrum of disease syndromes and the immune system is a major participant in malarial disease. This is particularly true in relation to the immune responses elicited against blood stages of -parasites that are responsible for the pathogenesis of infection. Mouse models of malaria are commonly used to dissect the immune mechanisms underlying disease.

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CD4 follicular helper T (Tfh) cells play a vital role in providing help for B cells undergoing selection and differentiation into activated antibody-secreting cells in mammalian germinal centers (GCs). Increasing evidence suggests that Tfh cells are a heterogeneous population that generates cytokine-skewed immune responses - a reflection of the microenvironment during differentiation. This has important ramifications for Tfh-mediated B cell help.

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It is widely accepted that infection and immune response incur significant metabolic demands, yet the respective demands of specific immune responses to live pathogens have not been well delineated. It is also established that upon activation, metabolic pathways undergo shifts at the cellular level. However, most studies exploring these issues at the systemic or cellular level have utilized pathogen associated molecular patterns (PAMPs) that model sepsis, or model antigens at isolated time points.

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Dendritic cells (DC) are sentinels of the immune system, alerting and enlisting T cells to clear pathogenic threats. As such, numerous studies have demonstrated their effective uptake and proteolytic activities coupled with antigen processing and presentation functions. Yet, less is known about how these cellular mechanisms change and develop as myeloid cells progress from progenitor cells to more differentiated cell types such as DC.

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