title: Modulation of monocyte antigen-presenting capacity by tumour necrosis factor-alpha (TNF): opposing effects of exogenous TNF before and after an antigen pulse and the role of TNF gene activation in monocytes.
abstract: We have previously shown that exogenous human recombinant tumour necrosis factor-alpha (rTNF), added before an antigen pulse, enhanced antigen presentation by human blood monocytes. The present study shows that, surprisingly, rTNF added after an antigen (PPD) pulse inhibited, while anti-TNF monoclonal antibody (mAb) enhanced, antigen presentation. mAbs htr-9 against p55 TNF receptor type I (TNF-RI) abrogated rTNF enhancing effect on PPD presentation and decreased presenting activity of untreated monocytes while utr-1 mAb, against p75 TNF receptor type II (TNF-RII), reversed the inhibitory effect of rTNF given after antigen pulse. PPD and rTNF when added singly induced TNF-mRNA accumulation in monocytes. Pretreatment of monocytes with rTNF followed by a PPD pulse caused an enhancement of TNF-mRNA accumulation. However, when post-treatment with rTNF was applied to PPD-pulsed monocytes, then inhibition of TNF gene expression was seen. This may point to the role of endogenously generated TNF in regulation of antigen-presenting capacity of monocytes. These studies indicate that TNF is an important regulator of monocyte antigen-presenting capacity and that the level of TNF gene activation in monocytes may be associated with their ability to present nominal antigen.
authors.affiliation: Department of Clinical Immunology, Polish-American Institute of Paediatrics, Jagiellonian University Medical College, Cracow.
authors.forename: D
authors.initials: D
authors.lastname: Kowalczyk
authors.forename: B
authors.initials: B
authors.lastname: Mytar
authors.forename: M
authors.initials: M
authors.lastname: Jasiński
authors.forename: J
authors.initials: J
authors.lastname: Pryjma
authors.forename: M
authors.initials: M
authors.lastname: Zembala
mesh_terms: D000911:Antibodies, Monoclonal / Q000276:immunology; D000938:Antigen-Presenting Cells / Q000276:immunology*; D002478:Cells, Cultured; D006801:Humans; D009000:Monocytes / Q000276:immunology*; D012333:RNA, Messenger / Q000096:biosynthesis; D018124:Receptors, Tumor Necrosis Factor / Q000096:biosynthesis / Q000502:physiology; D011994:Recombinant Proteins / Q000494:pharmacology; D014373:Tuberculin / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000008:administration & dosage / Q000235:genetics / Q000494:pharmacology / Q000502:physiology*; D015854:Up-Regulation / Q000187:drug effects / Q000502:physiology
chemical_list: D000911:Antibodies, Monoclonal; D012333:RNA, Messenger; D018124:Receptors, Tumor Necrosis Factor; D011994:Recombinant Proteins; D014373:Tuberculin; D014409:Tumor Necrosis Factor-alpha