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OP0267 The influence of latent cytomegalovirus (CMV) infection on T-cell-phenotype in children with juvenile idiopathic arthritis (JIA)
  1. R.D. Trippen,
  2. G. Almanzar,
  3. K. Sustal,
  4. K. Höfner,
  5. M. Prelog
  1. Department of Pediatrics, University of Wuerzburg, Wuerzburg, Germany


Background Life-long latent CMVinfection seems to diminish the size of the naive and the early memory T-cell pool and to drive Th1 polarization within the immune system. Previous studies in patients with Juvenile idiopathic arthritis (JIA) have shown that CMV-positive patients did not show an increase of CD28 effector T-cells compared to CMV-positive controls

Objectives The aim of this study was to determine the influence of latent CMV infection on the phenotype and cytokine profile of T-cell populations in children with JIA.

Methods Peripheral blood mononuclear cells (PBMC) and serum samples were obtained from 16 JIA patients in clinical remission on medication and 18 age-matched healthy donors (HD). Serum CMV-IgG concentration was determined by ELISA. So far, phenotypical characterization of peripheral T-cells was performed in CMV-positive (n=9) and CMV-negative (n=7) patients by flowcytometry.

Results The proportion of memory T-cells (CD45RACD28+CCR7+/–) within the CD4+ T-cell pool was significantly increased in CMV-positive patients (mean 47.4±16.6%) compared to CMV-negative patients (mean 32.9±7.4%) (p<0.05). In contrast, the proportion of naive T-cells (CD45RA+CD28+CCR7+) (CMV+: 37.3±18%; CMV-: 46.1±10.9%) within the CD4+ T-cell pool, the proportion of effector-memory T-cells (CD45RACD28-CCR7+/–) andterminal differentiated effector T-cells (CD45RA+CD28CCR7+/–) did not show a significant differences depending on the CMV-status. So far, no difference in the CMVpp65-specific IFN-gamma response could be found between JIA patients in remission and healthy controls.

Conclusions Our preliminary findings indicate a different T-cell response in CMV-positive JIA patients as found in CMV-positive healthy controls, possibly suggesting a disturbed peripheral T-cell response to latent CMV infection. So far it is unclear, whether these findings are primarily caused by the disease itself or secondarily to treatment and whether CMV may accelerate T-cell differentiation in JIA patients as described for healthy individuals. This may be of relevance for immune reconstitution of the immune system under T-cell-depleting therapies or during aging of JIA patients.

Disclosure of Interest None Declared

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