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Multicentric Castleman disease is associated with polyfunctional effector memory HHV-8-specific CD8+ T cells

Amélie Guihot1, Eric Oksenhendler, Lionel Galicier

  • 1Laboratoire d'Immunologie Cellulaire, Hôpital Pitié-Salpêtrière, Assistance Publique-Hôpitaux de Paris, Institut National de la Santé et de la Recherche Médicale, Université Pierre et Marie Curie Paris 6, Paris, France.

Blood
|November 15, 2007
PubMed

Insights

Multicentric Castleman disease (MCD) involves altered human herpesvirus 8 (HHV-8)-specific CD8(+) T cells. These cells show increased late-stage differentiation in MCD patients, correlating with viral load.

Area of Science:

  • Immunology
  • Virology
  • Oncology

Background:

  • Multicentric Castleman disease (MCD) is a severe lymphoproliferative disorder linked to human herpesvirus 8 (HHV-8) in immunocompromised individuals.
  • Understanding the immune response, particularly CD8(+) T cells, is crucial for elucidating MCD pathogenesis.

Purpose of the Study:

  • To investigate the characteristics of HHV-8-specific CD8(+) T cells in MCD patients compared to asymptomatic HHV-8 carriers (AC).
  • To assess the frequency, antigenic repertoire, differentiation, and functional capacity of these T cells.

Main Methods:

  • ELISpot assays using 56 peptides from HHV-8 proteins to screen CD8(+) T-cell responses.
  • Intracellular cytokine staining (IFN-gamma) and flow cytometry to analyze T-cell phenotypes (CD45RA, CCR7, CD27).
  • Correlation analysis between HHV-8 viral load and T-cell populations.

Main Results:

  • MCD and AC patients exhibited similar magnitudes and antigenic repertoires of HHV-8-specific CD8(+) T-cell responses.
  • A novel HLA-B7-restricted 10-mer epitope in HHV-8 K15 was identified.
  • MCD patients showed a distinct T-cell phenotype with significantly more late-differentiated (CD45RA(-)CCR7(-)CD27(-)) and fewer early/intermediate (CCR7(-)CD27(+)CD45RA(-)) effector memory cells compared to AC.
  • This phenotypic shift was specific to HHV-8 and not observed for Epstein-Barr virus-specific T cells.
  • Higher HHV-8 viral loads negatively correlated with early and intermediate effector memory T cells.
  • HHV-8-specific T cells in both groups were polyfunctional, secreting multiple cytokines (IFN-gamma, TNF-alpha, MIP-1beta) and expressing CD107a.

Conclusions:

  • MCD pathogenesis is not characterized by a deficiency or functional limitation of HHV-8-specific CD8(+) T cells.
  • The differentiation state of these T cells is influenced by HHV-8 viral load.
  • These findings provide novel insights into the immune mechanisms underlying MCD.

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