Immune escape driven by selection pressure from virus-specific CD8 T cells has been demonstrated in both chimpanzees and humans infected with the hepatitis C virus (HCV). Although escape mutations have also been characterized in major histocompatibility complex (MHC) class II-restricted HCV epitopes
In situ immune responses in Crohn's disease: A comparison with acute and persistent measles virus infection
β Scribed by Wakefield, A. J.; Sim, R.; Akbar, A. N.; Pounder, R. E.; Dhillon, A. P.
- Publisher
- John Wiley and Sons
- Year
- 1997
- Tongue
- English
- Weight
- 927 KB
- Volume
- 51
- Category
- Article
- ISSN
- 0146-6615
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β¦ Synopsis
The implied aetiological association of measles virus with Crohn's disease would be supported
The granuloma of Crohn's disease is an early, angioby detection of an immune response to infected centric inflammatory response , cells in affected tissues. This study sought to de-1991] and is likely to represent a transient tissue reactect and characterise in situ immune responses tion, possibly to foreign antigen. Despite being most to measles virus in both acutely and persistently frequently submucosal in location, the majority of iminfected tissues, and in particular, Crohn's granumunological studies of this condition have concentrated lomata. Tissue sections from patients with upon mucosal immune responses [Strober and James, Crohn's disease (n Ο 17), tuberculosis (n Ο 9), 1986]. A potential disadvantage of this approach is that acute intestinal ischaemia (n Ο 5), acute measles the inflamed mucosa may manifest a diversity of impneumonitis (n Ο 2), acute measles appendicitis mune responses that are consequent upon secondary (n Ο 1), subacute sclerosing panencephalitis translocation of luminal antigen. In contrast, mural (SSPE; n Ο 1), and measles inclusion body engranulomata are more likely to represent a specific reaccephalitis (MIBE; n Ο 1), were examined. Single tion to, what may be, a causative agent, especially when and double immunohistochemical labelling was these are located in deep layers of the gut, remote from performed to identify both cytotoxic lymphoulcerated sites. Recent studies from the UK [Wakefield cytes (CD8, TIA, perforin, Leu 7, CD45RO, et al., 1993; Lewin et al., 1995], Sweden [Ekbom et al., CD45RA) and macrophages (KP1). The relation-1994], and Japan , have implicated ship of these cells to measles infected cells was persistent measles virus infection as an aetiological examined by double immunolabelling with antiagent in inflammatory bowel disease, and live attentumeasles virus nucleoprotein antibody. In both ated measles vaccine has also be implicated in this conacute measles appendicitis and SSPE, CD8 Ο© /TIA Ο© text . cytotoxic lymphocytes (CTL) targeted infected Whereas cytotoxic T lymphocyte (CTL) responses are cells. In the cases of Crohn's disease (13/17), a feature of virtually all common acute virus infections, MIBE, fatal pneumonitis, and one tuberculous persistent virus infection may result from either a failgranuloma, that were positive for measles virus, ure to induce an adequate CTL response (low zone tolerinfected cells appeared to be targeted by macroance), or following an exhaustion of specific cytotoxicity phages rather than CTL. CTL in both tuberculous (high zone tolerance), during the primary infection and Crohn's granulomata were similar in their . We hypothesise that Crohn's peripheral distribution, number, and phenotype.
disease, in particular, may develop from a low zone The data suggest that measles-specific CTL retolerance with persistent infection, following either low sponses may be attenuated in Crohn's disease dose or attenuated measles virus infection early in life compared with acute measles appendicitis and [Ekbom et al., 1994;. SSPE, and secondly, that an abnormal macro-Ultrastructural studies of Crohn's disease have rephage response to persistent measles virus vealed apparent CTL adherence to, and polarisation of infection of the intestine may result in granulomatous inflammation.
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