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iNKT and memory B-cell alterations in HHV-8 multicentric Castleman disease.

iNKT and memory B-cell alterations in HHV-8 multicentric Castleman disease.
Author Information (click to view)

Sbihi Z, Dossier A, Boutboul D, Galicier L, Parizot C, Emarre A, Hoareau B, Dupin N, Marcelin AG, Oudin A, Fieschi C, Agbalika F, Autran B, Oksenhendler E, Carcelain G,


Sbihi Z, Dossier A, Boutboul D, Galicier L, Parizot C, Emarre A, Hoareau B, Dupin N, Marcelin AG, Oudin A, Fieschi C, Agbalika F, Autran B, Oksenhendler E, Carcelain G, (click to view)

Sbihi Z, Dossier A, Boutboul D, Galicier L, Parizot C, Emarre A, Hoareau B, Dupin N, Marcelin AG, Oudin A, Fieschi C, Agbalika F, Autran B, Oksenhendler E, Carcelain G,

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Blood 2016 11 09129(7) 855-865 doi 10.1182/blood-2016-06-719716

Abstract

Human herpesvirus 8 (HHV-8) is the causative agent of Kaposi sarcoma (KS) and multicentric Castleman disease (MCD), a life-threatening, virally induced B-cell lymphoproliferative disorder. HHV-8 is a B-lymphotropic γ-herpesvirus closely related to the Epstein-Barr virus (EBV). Invariant natural killer T (iNKT) cells are innate-like T cells that play a role in antiviral immunity, specifically in controlling viral replication in EBV-infected B cells. Decline of iNKT cells is associated with age or HIV infection, both situations associated with HHV-8-related diseases. We analyzed iNKT cells in both blood (n = 26) and spleen (n = 9) samples from 32 patients with HHV-8 MCD and compared them with patients with KS (n = 24) and healthy donors (n = 29). We determined that both circulating and splenic iNKT cell frequencies were markedly decreased in patients with HHV-8 MCD and were undetectable in 6 of them. Moreover, iNKT cells from patients with HHV-8 MCD displayed a proliferative defect after stimulation with α-galactosylceramide. These iNKT cell alterations were associated with an imbalance in B-cell subsets, including a significant decrease in memory B cells, particularly of marginal zone (MZ) B cells. Coculture experiments revealed that the decrease in iNKT cells contributed to the alterations in the B-cell subset distribution. These observations contribute to a better understanding of the complex interactions between HHV-8 and immune cells that cause HHV-8-related MCD.

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