作者: Hajime Kawamura , Jay A. Berzofsky , Shoichi Ozaki , Jena York-Jolley
DOI: 10.1016/0008-8749(87)90079-7
关键词: Cell biology 、 Major histocompatibility complex 、 Antigen-presenting cell 、 Lymphokine 、 Biology 、 Antigen presentation 、 T lymphocyte 、 Antigen 、 Cytotoxic T cell 、 Immunology 、 Immune system
摘要: Myoglobin-specific, Iad-restricted cloned helper T cells and hybridomas were found to directly kill Iad-bearing, myoglobin-pulsed B lymphoma targets could also bystander targets, but only in the presence of antigen-pulsed antigen presenting (APC). The induction killing requires recognition processed context class II major histocompatibility complex (MHC) molecules. Despite specificity induction, suggests a nonspecific lytic mechanism. direct can be inhibited by cold specific whereas blocked both targets. target inhibition seems due interference with effector-to-target contact or proximity rather than high-dose suppression T-cell activation. Experiments using supernatants cyclosporin A suggested that synthesizing short-range soluble factor(s) activity de novo during effector phase, while antigen-specific signal transduction is occurring. mechanism appears absorption consumption short-acting cytotoxic lymphokine which must able interact closely cell. Normal spleen cells, despite their capability for activating cannot inhibit killed even after lipopolysaccharide stimulation. Thus, although may play negative feedback role normal immune response, our data raise possibility T-cell-mediated contribute surveillance against malignancy virtue preferential tumor either indirectly.