Cell interactions in alveolar macrophage-mediated suppression of the immune response: An unusual suppressor pathway involving a population of T-cells that express Lyt-1, L3T4, and I-J

• Published in: Cellular immunology Vol. 116; no. 1; pp. 183 - 194
• Main Authors: Ferrick, David A., Herscowitz, Herbert B.
• Format: Journal Article
• Language: English
• Published: San Diego, CA Elsevier Inc 01.10.1988; Elsevier
• Subjects: Analysis of the immune response. Humoral and cellular immunity; Animals; Antibodies, Monoclonal; Antibody Formation; Antigens, Differentiation, T-Lymphocyte - analysis; Antigens, Ly - analysis; Biological and medical sciences; Cell interactions; Cell Separation; Fundamental and applied biological sciences. Psychology; Fundamental immunology; Histocompatibility Antigens Class II - analysis; Immune Tolerance; Immunity, Cellular; Immunobiology; Macrophages - immunology; Mice; Mice, Inbred C57BL; Pulmonary Alveoli - cytology; T-Lymphocytes, Regulatory - classification; T-Lymphocytes, Regulatory - immunology; Immune response; Lung; Rodentia; Cell cell interaction; Splenocyte; Hemolytic plaque test; In vitro; Cell subpopulation; Vertebrata; Mixed cell culture; Immunosuppression; Mammalia; Mouse; T-Lymphocyte; Macrophage
• ISSN: 0008-8749; 1090-2163
• DOI: 10.1016/0008-8749(88)90220-1

Studies from this laboratory have demonstrated that incubation of murine alveolar macrophages (AM) with SRBC-primed spleen cells (SC) results in suppression of the in vitro plaqueforming cell (PFC) response and that suppression is mediated by a soluble factor contained in supernatants obtained from cultures of AM and SC. In the present study, immunological techniques employing monoclonal antibody (MoAb) were used to isolate various T-cell subsets in order to determine the phenotype of the cells which interact with AM to produce suppression. Spleen cell populations depleted of Thy-1 +-, Lyt-1 +-, L3T4 +-, or I-J +-bearing cells failed to generate suppressive supernatants when cultured with AM. Depletion of Lyt-2 + T-cells (the classical suppressor/effector subset) did not alter the ability of the remaining cell population to cooperate with AM for generation of suppressive supernatants. Direct suppression of the PFC response in cultures containing AM was abrogated after treatment of the spleen cells with anti-I-J, but not anti-Lyt-2 MoAbs. Reconstitution of the AM-mediated suppressive response with enriched populations of SC required the presence of T-cells which expressed Lyt-1, L3T4, and I-J. These results suggest the existence of an unusual suppressor pathway involving I-J restriction but which appears to be mediated by the interaction of AM with a population of T-cells that expresses surface markers characteristic of T-helper cells.