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Expression of the interferon‐inducible chemokine IP‐10 (CXCL10), a chemokine with proposed anti‐neoplastic functions, in Hodgkin lymphoma and nasopharyngeal carcinoma
Author(s) -
Teichmann Martina,
Meyer Birgit,
Beck Andreas,
Niedobitek Gerald
Publication year - 2005
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.1745
Subject(s) - nasopharyngeal carcinoma , cxcr3 , biology , lymphoma , chemokine , epstein–barr virus , chemokine receptor , cxcl10 , cancer research , metastasis , immunology , immune system , virus , medicine , cancer , radiation therapy , genetics
Hodgkin lymphoma (HL) and nasopharyngeal carcinoma (NPC) are characterized by their association with Epstein–Barr virus (EBV) and an abundant infiltrate of reactive lymphoid cells. The presence of this lymphoid stroma may influence the effect of anti‐viral immunotherapy. The interferon‐inducible chemokine IP‐10 has anti‐neoplastic effects in several model systems mediated by T‐cells expressing the CXCR3 chemokine receptor. Using in situ hybridization, it is shown that IP‐10 is expressed in neoplastic cells of HL and correlates both with the mixed cellularity histotype and with EBV infection. IP‐10 expression was also detected in tumour cells of most NPCs as well as in EBV‐negative squamous cell carcinomas of the tongue. Thus, in carcinomas, IP‐10 expression showed no correlation with EBV infection. Numerous CXCR3‐positive lymphocytes were detected in the lymphoid stroma of HL and NPC, raising the possibility of a Th1‐predominant immune response in these cases. In view of the proposed anti‐neoplastic functions of IP‐10 and CXCR3‐positive lymphocytes, these findings are unexpected and raise the possibility that endogenous IP‐10 expression in the context of human tumours may not exert the anti‐tumour effects ascribed to it by in vitro experiments. Copyright © 2005 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.