1989
DOI: 10.1016/0016-5085(89)90406-x
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Immunobiology and immunopathology of human gut mucosa: Humoral immunity and intraepithelial lymphocytes

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Cited by 529 publications
(293 citation statements)
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“…Intestinal lamina propria-associated lymphocytes constitute a major lymphoid compartment, continuously exposed to heavy antigen challenge in vivo (1,2). Persistent antigen-induced lymphocyte activation does not normally result in inflammatory tissue damage, suggesting the existence of mechanisms responsible for regulating local immune responses.…”
Section: Introductionmentioning
confidence: 99%
“…Intestinal lamina propria-associated lymphocytes constitute a major lymphoid compartment, continuously exposed to heavy antigen challenge in vivo (1,2). Persistent antigen-induced lymphocyte activation does not normally result in inflammatory tissue damage, suggesting the existence of mechanisms responsible for regulating local immune responses.…”
Section: Introductionmentioning
confidence: 99%
“…The IEL population of cattle, similar to those of other species Brandtzaeg et al, 1989), consisted of a majority of T cells, a large proportion of which were CD8 +. This phenotypic profile suggests that certain functional subsets of lymphocytes may preferentially migrate into the epithelial compartment.…”
Section: Discussionmentioning
confidence: 75%
“…By contrast, the intraepithelial lymphocyte (IEL) population is characterized by a high percentage of CD8 ÷ T cells . Since the IELs are located at the interface between the host and the environment, it has been proposed that they participate in the first line of defence against enteric pathogens or in the maintenance of mucosal homeostasis by regulating the response to dietary antigens (Brandtzaeg et al, 1989). The IELs are present in all vertebrate species and constitute a significant proportion of the total lymphocyte population, suggesting that they are likely to be an important component of host defence (Fichtelius et al, 1969).…”
Section: Introductionmentioning
confidence: 99%
“…There are important parallels in animal models of allograft rejection and graft-ver5w.s-host disease to the range of mucosal lesions seen in coeliac disease [14], suggesting that these lesions arise from the sensitization of mucosal T cells [15,16]. Further evidence to support a cellmediated immune response in the pathogenesis of coeliac disease comes from the observation that in untreated coeliac disease a significantly increased number of infiltrating T cells carry the CD45RO marker [17], suggesting an influx of antigenprimed memory cells [2,18]. Both aP and 76 T cells are involved in this immune response, and have been shown to undergo activation and proliferate following challenge with gluten in vivo [19].…”
Section: Discussionmentioning
confidence: 99%