Publications by authors named "Felix Odhiambo Hayara"
Background: Helminth infections can modulate immunity to Mycobacterium tuberculosis (Mtb). However, the effect of helminths, including Schistosoma mansoni (SM), on Mtb infection outcomes is less clear. Furthermore, HIV is a known risk factor for tuberculosis (TB) disease and has been implicated in SM pathogenesis.
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- Schistosoma mansoni (SM) is a widespread parasitic infection affecting over 200 million people, and its complex life cycle elicits varying immune responses during different stages, particularly highlighting the limited knowledge of adult worm responses.
- Research focused on how co-infection with Mycobacterium tuberculosis (Mtb) alters the T cell response to SM in a study group from Kisumu, Kenya, revealed that γδ T cells were more active in responding to worm antigens than egg antigens.
- The results indicated that Mtb infection dampens the proliferation of γδ T cells to SM worm antigens while increasing IL-4 production, suggesting that Mtb modifies the immune interaction with SM.
HIV infection is a significant risk factor for reactivation of latent infection (LTBI) and progression to active tuberculosis disease, yet the mechanisms whereby HIV impairs T cell immunity to have not been fully defined. Evaluation of -specific CD4 T cells is commonly based on IFN-γ production, yet increasing evidence indicates the immune response to is heterogeneous and encompasses IFN-γ-independent responses. We hypothesized that upregulation of surface activation-induced markers (AIM) would facilitate detection of human -specific CD4 T cells in a cytokine-independent manner in HIV-infected and HIV-uninfected individuals with LTBI.
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