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Eur J Immunol. 1988 Feb;18(2):211-8.

B-T lymphocyte interactions in experimental autoimmune myasthenia gravis: antigen presentation by rat/mouse hybridoma lines secreting monoclonal antibodies against the nicotinic acetylcholine receptor.

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Clinical Research Unit for Multiple Sclerosis, Max-Planck-Gesellschaft, Würzburg, FRG.


Many, but not all rat/mouse B hybridoma cells, producing monoclonal antibodies against determinants on the nicotinic acetylcholine receptor (AChR) of the electric organ of Torpedo californica, were able to immunologically present antigen to AChR-specific, Ia-compatible CD4+ T lymphocyte lines. Most of the hybridomas presented AChR in a privileged manner, i.e. they present AChR even more effectively than macrophages or dendritic cells. However, in the presentation of antigens other than AChR, they were inferior to macrophages. Moreover, some hybridomas were able to present AChR not only in soluble state, but also in membrane vesicles. Privileged presentation of AChR by hybridomas depended on the reactivity of the secreted immunoglobulins with epitopes of the AChR alpha chain, and on the expression of major histocompatibility complex class II antigens on the hybridoma cell surface. There was, however, no quantitative correlation between the actual AChR presentation capacity of one clone and the density of its surface Ia. Neither fine specificity nor isotype of hybridoma immunoglobulin are critical in determining privileged AChR presentation. We postulate that different hybridomas vary in their ability to take up soluble and particulate antigen, to process and to re-express them on the cellular membrane. This capacity may determine their efficiency to present antigen to T cells.

[Indexed for MEDLINE]

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