6533b822fe1ef96bd127cc15
RESEARCH PRODUCT
Major histocompatibility complex class I-restricted activation of cloned T cells by a soluble protein in the absence of accessory cells.
Angelika B. Reske-kunzThomas Dicksubject
MHC class IIMultidisciplinarybiologyOvalbuminT-LymphocytesHistocompatibility Antigens Class IAntigen presentationCD1chemical and pharmacologic phenomenaMHC restrictionLymphocyte ActivationVirologyMolecular biologyAntibodiesCell LineClone CellsMiceAntigenMHC class Ibiology.proteinAnimalsCytotoxic T cellAntigen-presenting cellResearch Articledescription
A T-cell clone, 10BK.1, was established from the draining lymph nodes of (B10 x B10.BR)F1 mice immunized with ovalbumin (OVA) according to standard protocols. Upon coculture with the antigen, 10BK.1 cells reacted by production of lymphokines and by proliferation despite the absence of additional antigen-presenting cells. These T cells do not express major histocompatibility complex (MHC) class II molecules on the cell surface as assessed on the basis of several criteria: by cytofluorometric analysis I-A and I-E determinants were not detectable; 10BK.1 cells could not act as antigen-presenting cells for long-term-cultured MHC class II-restricted T-cell clones; and monoclonal antibodies directed at both MHC class II isotypic complexes (I-A, I-E) did not suppress their OVA-induced activation. In contrast, proliferation of 10BK.1 T cells in response to OVA was abrogated by antibodies directed at H-2Kb antigens. Inhibition experiments employing antibodies directed at Lyt-2 and L3T4 antigens in addition to cytofluorometric analysis revealed that T-cell clone 10BK.1 exhibits the Thy-1+,Lyt-2+,Ly-1-,L3T4- phenotype. 10BK.1 cells pulsed with OVA and fixed with glutaraldehyde induced proliferation of untreated 10BK.1 cells. These data support the theory that 10BK.1 T cells present the exogenous globular protein OVA to one another in an MHC class I-restricted manner, resulting in cell activation and proliferation independent of added accessory cells.
year | journal | country | edition | language |
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1989-04-01 | Proceedings of the National Academy of Sciences |