Differential chemokine, chemokine receptor and cytokine expression in Epstein-Barr virus-associated lymphoproliferative diseases

Koichi Ohshima, Kennosuke Karube, Makoto Hamasaki, Takeshi Tutiya, Takahiro Yamaguchi, Hiroaki Suefuji, Keiko Suzuki, Junji Suzumiya, Shoichi Ohga, Masahiro Kikuchi

Research output: Contribution to journalArticle

26 Citations (Scopus)

Abstract

T cell immunity plays an important role in the clinicopathology of Epstein-Barr virus (EBV)-associated diseases. Acute EBV-induced infectious mononucleosis (IM) is a common self-limiting disease, however, other EBV-associated diseases, including chronic active EBV infection (CAEBV), NK cell lymphoma (NKL), and Hodgkin's lymphoma (HL), exhibit distinct clinical features. Chemokines are members of a family of small-secreted proteins. The relationships between chemokines and the chemokine receptor (R) are thought to be important for selectivity of local immunity. Some chemokines, chemokine R and cytokines closely associate with the T cell subtypes, Th1 and Th2 T cells and cytotoxic cells. To clarify the role of T cell immunity in EBV-associated diseases, we conducted gene expression profiling, using chemokine, chemokine R and cytokine DNA chips. Compared to EBV negative non-specific lymphadenitis, CAEBV and NKL exhibited diffuse down- and up-regulation, respectively, of these gene profiles. IM had a predominantly Th1-type profile, whereas HL had a mixed Th1/Th2-type profile. Reduction of the Th1-type cytokine interferon gamma (IFN-γ) in CAEBV was confirmed by Reverse transcriptase-polymerase chain reaction, whereas IFN-γ expression was markedly enhanced in NKL, and moderately enhanced in IM. Compared to IM, CAEBV showed slight elevation of "regulated upon activation, normal T expressed and secreted" (RANTES), but almost all other genes assayed were down-regulated. NKL exhibited elevated expression of numerous genes, particularly IFN-γ inducible-10 (IP-10) and monokine induced by IFN-γ (MIG). HL showed variable elevated and reduced expression of various genes, with increased expression of IL-13 receptor and MIG. Our study demonstrated the enormous potential of gene expression profiling for clarifying the pathogenesis of EBV-associated diseases.

Original languageEnglish
Pages (from-to)1367-1378
Number of pages12
JournalLeukemia and Lymphoma
Volume44
Issue number8
DOIs
Publication statusPublished - Aug 1 2003

All Science Journal Classification (ASJC) codes

  • Hematology
  • Oncology
  • Cancer Research

Fingerprint Dive into the research topics of 'Differential chemokine, chemokine receptor and cytokine expression in Epstein-Barr virus-associated lymphoproliferative diseases'. Together they form a unique fingerprint.

  • Cite this

    Ohshima, K., Karube, K., Hamasaki, M., Tutiya, T., Yamaguchi, T., Suefuji, H., Suzuki, K., Suzumiya, J., Ohga, S., & Kikuchi, M. (2003). Differential chemokine, chemokine receptor and cytokine expression in Epstein-Barr virus-associated lymphoproliferative diseases. Leukemia and Lymphoma, 44(8), 1367-1378. https://doi.org/10.1080/1042819031000082984