Repository hosted by TU Delft Library

Home · Contact · About · Disclaimer ·
 

Decreased sensitivity to dexamethasone in lymphocytes from patients with Alzheimer's disease

Publication files not online:

Author: Nijhuis, E. · Hinloopen, B. · Duijn, C. van · Hofman, A. · Rozing, J. · Nagelkerken, L.
Type:article
Date:1994
Institution: Section of Immunology, Inst. of Aging and Vascular Research, TNO, Leiden, Netherlands TNO Preventie en Gezondheid
Source:Clinical Immunology and Immunopathology, 1, 73, 45-52
Identifier: 232696
doi: doi:/10.1006/clin.1994.1168
Keywords: Health · cd4 antigen · dexamethasone · glucocorticoid · hydrocortisone · interleukin 2 · interleukin 4 · clinical article · clinical trial · controlled clinical trial · controlled study · Male · t lymphocyte subpopulation · Aged · Alzheimer Disease · Dexamethasone · Female · Humans · Lymphocyte Activation · Phenotype · Sensitivity and Specificity · T-Lymphocytes

Abstract

Cortisol levels in patients with Alzheimer's disease (AD) are relatively unaffected by a challenge with dexamethasone (DEX) in vivo. The present study demonstrates that DEX is less inhibitory for phytohemagglutinin (PHA)-induced T cell proliferation in AD patients as compared to age-matched controls. Since no significant differences were found between AD patients and age-matched controls with regard to the fraction of CD45RA+ or CD45RO+ CD4+ T cells nor the ability of peripheral blood mononuclear cells to produce IL-2 or IL-4, it is unlikely that the difference in DEX sensitivity is due to a changed lymphokine profile or a changed composition of the CD4+ T cell population. Sensitivity to DEX was negatively correlated with the ability to produce IL-2 and IL-4 in the controls but not in AD patients. This suggests that IL-2 and IL-4 synthesis in AD patients is less sensitive to regulation by glucocorticoids.