Influence of amitriptyline therapy on T cell phenotype in chronic pain patients.

Chronic pain (CP) is a major health issue globally, affecting millions and resulting in a significant healthcare burden. Although amitriptyline is widely used to manage CP, its immunomodulatory effects during pain therapy, especially on T cell phenotypes, remain unclear. In this study, we explored how amitriptyline alters T cell phenotypes in CP patients.

Red pulp macrophages clear parasites, while marginal metallophilic and marginal zone macrophages support CD4 T cell activation during infection.

Malaria, caused by the parasite spp., remains the most prevalent and dangerous vector-borne infectious disease worldwide. Effective pathogen clearance during malaria hinges on the interplay between adaptive and innate immune responses, especially on T cells, B cells, antigen-presenting cells (APCs) and IFNγ response.

Amitriptyline inhibits Plasmodium development in infected red blood cells by modulating sphingolipid metabolism and glucose uptake.

Malaria remains a global health challenge, necessitating novel therapeutic approaches. Here, we explore the role of the sphingolipid metabolism in Plasmodium infection. We focus on the enzyme acid sphingomyelinase (Asm), which hydrolyzes sphingomyelin to ceramide, a structural but also bioactive membrane molecule.

Direct effects of heroin and methadone on T cell function.

Opioid addiction presents a relevant health challenge, with chronic heroin use linked to detrimental effects on various aspects of physical, mental, and sociological health. Opioid maintenance therapy (OMT), particularly using methadone, is the primary treatment option for heroin addiction. Previous studies using blood samples from current heroin addicts and OMT patients have shown immunomodulatory effects of heroin and methadone on T cell function.