title: Secretion of colony-stimulating factors by T cell clones. Role in adoptive protection against Listeria monocytogenes.
abstract: CSF have been postulated to be important mediators of host defenses. The current studies were undertaken to investigate the production of CSF by Listeria-specific, T cell clones and to assess the participation of CSF in anti-listerial host resistance. Listeria-specific L3T4+, Lyt-2- T cell clones were isolated and expanded by standard techniques. The clones themselves protected mice from listerial challenge when injected intravenously, and supernatants generated from Ag-stimulated clones were protective. In order to define factors important in the protection, supernatants from the clones were assayed for CSF by several in vitro assays. Total colony-stimulating activity was measured with a bone marrow colony-forming assay. T cell clones secreted 1000 to 2000 U/ml of colony-stimulating activity after 48 hours of stimulation with specific antigen. The relative amounts of the various CSF were determined by the capacity of supernatants to support proliferation of the factor-dependent cell lines FDCP-1 and 32D cl 3 in the presence and absence of specific anti-CSF antibodies. Results showed that most of the CSF activity was due to granulocyte-macrophage (GM)-CSF and IL-3. The role of GM-CSF in anti-listerial host resistance was assessed in two types of experiments. In one set of experiments GM-CSF activity was neutralized in the supernatants by addition of specific rabbit anti-GM-CSF antibodies. Treated and untreated supernatants were then tested for their capacity to protect nonimmune mice against listerial challenge. Neutralization of GM-CSF in the supernatants decreased the protective capacity of the supernatants by approximately 23%. In a second set of studies, the administration of recombinant murine GM-CSF was shown to protect mice from challenges of L. monocytogenes. Taken together, these experiments provide evidence that CSF are important mediators of immune T cell mediated host defenses.
authors.affiliation: Department of Medicine, University of Texas Health Science Center, San Antonio 78284.
authors.forename: D M
authors.initials: DM
authors.lastname: Magee
authors.forename: E J
authors.initials: EJ
authors.lastname: Wing
mesh_terms: D000818:Animals; D002460:Cell Line; D002474:Cell-Free System; D002999:Clone Cells / Q000276:immunology / Q000378:metabolism / Q000637:transplantation; D003115:Colony-Stimulating Factors / Q000096:biosynthesis* / Q000276:immunology / Q000502:physiology; D005260:Female; D016178:Granulocyte-Macrophage Colony-Stimulating Factor; D006133:Growth Substances / Q000276:immunology; D007106:Immune Sera / Q000494:pharmacology; D007113:Immunity, Innate; D007116:Immunization, Passive; D008088:Listeriosis / Q000276:immunology; D008213:Lymphocyte Activation; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D009500:Neutralization Tests; D011817:Rabbits; D013601:T-Lymphocytes / Q000276:immunology / Q000378:metabolism* / Q000637:transplantation
chemical_list: D003115:Colony-Stimulating Factors; D006133:Growth Substances; D007106:Immune Sera; D016178:Granulocyte-Macrophage Colony-Stimulating Factor