Blocking the Induction of HLA Class II Expression by Thyroid Epithelial Cells In Vitro View Full Text


Ontology type: schema:Chapter     


Chapter Info

DATE

1991

AUTHORS

I. Todd , V. Guerin , G. F. Bottazzo

ABSTRACT

Cells expressing class II molecules of the major histocompatibility complex (MHC) have the potential, in the presence of antigen, to interact with CD4 + T lymphocytes which are mainly implicated in the induction of immune responses. This may help to explain the limited tissue distribution of HLA class II since it restricts the possibilities for immunological interactions to defined, controllable proportions. Thus, most tissue cells are normally HLA class II negative, and this includes thyroid epithelial cells (thyrocytes). By contrast, thyro-cytes of patients with autoimmune thyroid diseases frequently express HLA class II [1–3]. These cells, which are themselves the target of the autoimmune attack, may then interact with CD4 + T cells and thereby influence the autoimmune process. It has been hypothesised that the activation of helper T cells by such an interaction might stimulate the pathogenesis [4]. This is supported by the observations that thyroid-specific, autoreactive T cells can be stimulated in vitro by autologous [5–7] or syngeneic [8] thyrocytes bearing MHC class II. However, another possibility is raised by recent findings that the interaction of T cells with antigen plus MHC in the absence of “accessory signals” can induce a state of anergy in the T cells (referenced in [9]). Thus it is feasible that MHC class II positive thyrocytes might in some circumstances down-regulate rather than stimulate the activity of thyroid autoreactive T cells [10] if the required accessory signals are not provided. More... »

PAGES

239-247

References to SciGraph publications

Book

TITLE

Autoimmune Thyroiditis

ISBN

978-3-540-53476-1
978-3-642-76301-4

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/978-3-642-76301-4_28

DOI

http://dx.doi.org/10.1007/978-3-642-76301-4_28

DIMENSIONS

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