Editor,—What is one to make of the immunohistochemical study of Iizuka et al ( Gut 2000; 46: 163–169 OpenUrlCrossRefPubMedWeb of Science)? Before addressing the possible scientific implications of their findings, it is worth clarifying a few points with respect to our own research. Iizukaet al state that “the measles hypothesis is based on the theory that measles antibody recognises measles virus itself and the measles virus antigen is uniquely present in Crohn's disease.” Is this the authors' hypothesis? It is certainly not ours. That the measles antibody used in our studies (not that used by the authors in the present study) recognises the measles virus is not in doubt. The appropriate question is “does the antibody detect human antigenic epitopes in addition to measles virus N-protein?” Specificity studies in our own laboratory, including application to mixed preparations of measles virus infected and uninfected cells, application to cell lines infected with other viruses, and tissue studies incorporating in situ hybridisation (ISH) and combined ISH-reverse transcription-polymerase chain reaction (RT-PCR)-ISH for measles virus N-gene in serial tissue sections of infected human tissues suggest that the antibody, when used appropriately, is specific for measles virus.

Our own hypothesis relates not to the unique presence of measles in Crohn's disease but rather to the specific localisation of the virus to the hallmark lesions of this disease—granulomas and secondary lymphoid reactions—that are themselves a likely response to persistent and potentially causative antigen(s). While the focus of our studies has been the exclusive presence of viral antigen in these foci in Crohn's disease, Iizuka et al have assiduously avoided these pathological structures altogether. Instead, they have identified a pattern of non-specific …

M Iizuka, First Department of Internal Medicine, Akita University School of Medicine, 1–1–1 Hondo, Akita 010–8543, Japan.iizuka{at}med.akita-u.ac.jp