title: Cooperation between humoral factor(s) and Lyt-2+ T cells in effective clearance of Sendai virus from infected mouse lungs.
abstract: The mechanism of cooperation between the L3T4+ and Lyt-2+ T cell subsets in effective clearance of Sendai virus from infected mouse lungs was studied by adoptive cell transfer using nude mice. Simultaneous transfer of a long-term-cultured Sendai virus-specific L3T4+ T cell line with L3T4+ cell-depleted immune spleen cell (L3T4-) fraction to infected nude mice could result in viral clearance, although single injection with either of these cells was not effective. Instead of the L3T4+ T cells, culture supernatants of the L3T4- T cell line or concanavalin A-stimulated mouse spleen cells and mouse serum immunized with the virus were also active in the cooperative viral clearance with L3T4- fraction. The role of the Sendai virus-sensitized L3T4- cell fraction in cooperative viral clearance with humoral factors could be replaced by neither T cell-deprived immune spleen cell fraction nor normal spleen cells. The 1,500 units of recombinant mouse interleukin 2 (IL-2), which was more than 12 times the IL-2 activity present in the supernatants of the T cell line or concanavalin A-stimulated spleen cells, failed to clear the virus in combination with the L3T4- fraction. Monoclonal antibodies to Sendai or mouse hepatitis viruses were also effective in the cooperative antiviral activity. IL-2 activity was not detected in these monoclonal antibodies and the mouse immune serum. Single injection of any humoral factors failed to clear the virus. These results indicate that Sendai virus-sensitized Lyt-2+ subset of T cells acts cooperatively with humoral factor(s) other than IL-2 or Sendai virus-specific antibody present in supernatants of the T cell line, of concanavalin A-stimulated spleen cells or hybridomas, and in mouse serum immunized with the virus.
authors.affiliation: Department of Veterinary Public Health, Institute of Public Health, Tokyo.
authors.forename: H
authors.initials: H
authors.lastname: Iwai
authors.forename: S
authors.initials: S
authors.lastname: Yamamoto
authors.forename: Y
authors.initials: Y
authors.lastname: Otsuka
authors.forename: K
authors.initials: K
authors.lastname: Ueda
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000276:immunology; D000914:Antibodies, Viral / Q000276:immunology; D000950:Antigens, Ly / Q000032:analysis; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D002460:Cell Line; D007109:Immunity; D007116:Immunization, Passive; D007376:Interleukin-2 / Q000494:pharmacology; D008168:Lung / Q000276:immunology*; D008213:Lymphocyte Activation; D008211:Lymphocyte Cooperation; D008222:Lymphokines / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D010222:Parainfluenza Virus 1, Human / Q000276:immunology*; D018184:Paramyxoviridae Infections / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology*
chemical_list: D000911:Antibodies, Monoclonal; D000914:Antibodies, Viral; D000950:Antigens, Ly; D007376:Interleukin-2; D008222:Lymphokines