Expression of B7 (CD80) and CD40 antigens and the CD40 ligand in Hodgkin's disease is independent of latent Epstein--Barr virus infection
Autor: | J Oates, J Crocker, Paul Murray, G M Reynolds, L S Young |
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Rok vydání: | 1995 |
Předmět: |
CD40
biology business.industry chemical and pharmacologic phenomena hemic and immune systems medicine.disease Ligand (biochemistry) Virus Pathology and Forensic Medicine Antigen immune system diseases hemic and lymphatic diseases Papers Immunology medicine Cancer research biology.protein Immunohistochemistry business Antigen-presenting cell Epstein–Barr virus infection CD80 |
Zdroj: | Molecular Pathology. 48:M105-M108 |
ISSN: | 1366-8714 |
Popis: | Aim —To examine the expression of CD40 and B7 (CD80) antigens and the CD40 ligand in Hodgkin9s disease. Methods —Antigen and ligand expression was studied in 17 cases of Hodgkin9s disease using immunohistochemistry. The study included 11 cases of Hodgkin9s disease in which latent Epstein-Barr virus (EBV) infection could be demonstrated within tumour cells by in situ hybridisation for the EBV encoded early RNAs (EBERs). Results —In all cases, irrespective of EBV status, Reed-Sternberg cells and their variants (HRS cells) showed strong expression of both B7 and CD40 antigens. CD40 ligand expression was not shown in HRS cells but was confined to a subset of small lymphocytes some of which were seen to be in intimate contact with HRS cells. Paraffin wax sections from a further 60 cases of Hodgkin9s disease were examined for CD40 and EBER expression alone. The CD40 antigen was identified in HRS cells in all of these cases irrespective of EBER expression. Conclusions —As CD40 and B7 expression are features of professional antigen presenting cells, these results provide further evidence that HRS cells may have antigen presenting properties and that this may contribute to the characteristic recruitment and activation of non-malignant lymphocytes which is a feature of Hodgkin9s disease. The ability of HRS cells to activate T h cells may in turn contribute to their own survival through the induction of the gp39/CD40 pathway. |
Databáze: | OpenAIRE |
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