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Dissociation among Ia antigen expression, accessory cell function, and antigen processing in two acute monoblastic leukemia lines.

Abstract：

:To better understand the role of Ia antigen expression, accessory cell function, and antigen ingestion in antigen presentation and the initiation of T cell proliferation, we studied these events in two acute monoblastic leukemia (AMoL) lines. The cell lines were positive for surface Ia antigen; one stimulated proliferation of the allogeneic mononuclear cells in mixed lymphocyte culture and culture supernatants from the other line contained interleukin 1 (IL-1) when tested for comitogen activity in a standard mouse thymocyte assay. The AMoL cells also contributed accessory factors for mitogen-induced proliferative responses by T cells. High numbers of cells of one of the lines tended to suppress mitogen induced T cell proliferation. Irradiated trinitrophenylated AMoL cells were able to stimulate TNP-specific HLA-DR matched T cell blasts to proliferate. However, when irradiated AMoL cells were cultured with a protein antigen (tetanus toxoid or varicella zoster) plus antigen-specific parental T cell blasts, antigen presentation failed to occur. Diminished phagocytosis by the AMoL cells, together with reduced catabolism of labelled antigen, is a likely explanation for this finding. Our results demonstrate that the concurrent presence of a complex protein antigen and Ia-positive monocytic leukemia cells capable of accessory function is alone insufficient to maintain antigen-specific T cell proliferation. Moreover, these findings suggest that antigen processing, involving ingestion and reexpression of antigenic determinants, is an essential aspect of antigen presentation not tightly linked to Ia antigen expression or IL-1 production in these AMoL lines.

journal_name

J Clin Immunol

journal_title

Journal of clinical immunology

authors

Giller RH,Mori M,Hayward AR

doi

10.1007/BF00916572

subject

Has Abstract

pub_date

1984-11-01 00:00:00

pages

429-38

issue

6

eissn

0271-9142

issn

1573-2592

journal_volume

4

pub_type

杂志文章

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