Objective: To test the hypothesis that T treatment withdrawal could be associated with an enhancement of proinflammatory cytokine production by peripheral blood monocytes and dendritic cells.
Design: A prospective intervention study.
Setting: Tertiary university hospital.
Patient(s): Thirteen type 2 diabetic men aged >55 years with partial androgen deficiency and eight age-matched healthy men (controls).
Intervention(s): Analyses were performed before and 12 months after T replacement therapy and the results compared with those obtained for the same patients after a 3-month T withdrawal period.
Main Outcome Measure(s): Distribution of circulating T, B, and natural killer lymphocytes, monocytes, and CD33(hi) myeloid, CD16+, and plasmacytoid dendritic cell subsets. Spontaneous and stimulated ex vivo production of inflammatory cytokines (interleukin-1beta, interleukin-6, and tumor necrosis factor-alpha) by circulating monocytes and dendritic cells, which represent the most potent antigen-presenting cells.
Result(s): The reduction or complete abrogation of spontaneous ex vivo production of proinflammatory cytokines by monocytes and dendritic cells observed after 12 months of T replacement therapy was maintained 3 months after T withdrawal.
Conclusion(s): These are the first results showing that exogenous T treatment deprivation is not associated with an immunologic enhancement of proinflammatory cytokine production by antigen-presenting cells.
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http://dx.doi.org/10.1016/j.fertnstert.2008.05.040 | DOI Listing |
Brain Behav Immun Health
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Department of Health Sciences, Interdisciplinary Research Center of Autoimmune Diseases-IRCAD, University of Eastern Piedmont, 28100, Novara, Italy.
Major Depressive Disorder (MDD) is a widespread psychiatric condition impacting social and occupational functioning, making it a leading cause of disability. The diagnosis of MDD remains clinical, based on the Diagnostic and Statistical Manual of Mental Disorders (DSM)-5 criteria, as biomarkers have not yet been validated for diagnostic purposes or as predictors of treatment response. Traditional treatment strategies often follow a one-size-fits-all approach obtaining suboptimal outcomes for many patients who fail to experience response or recovery.
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IrsiCaixa, Badalona, Spain.
Introduction: HIV-1 exploits dendritic cells (DCs) to spread throughout the body via specific recognition of gangliosides present on the viral envelope by the CD169/Siglec-1 membrane receptor. This interaction triggers the internalization of HIV-1 within a structure known as the sac-like compartment. While the mechanism underlying sac-like compartment formation remains elusive, prior research indicates that the process is clathrin-independent and cell membrane cholesterol-dependent and involves transient disruption of cortical actin.
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