High dose suppression of human anti-influenza A virus responses using T cell clones

• Published in: Immunology and cell biology Vol. 65 ( Pt 1); p. 25
• Main Authors: Adams, E, Wotherspoon, J, Hellqvist, L, Basten, A
• Format: Journal Article
• Language: English
• Published: United States 01.02.1987
• Subjects: Antibodies, Viral - biosynthesis; Antigens, Viral - immunology; Clone Cells - immunology; Humans; Influenza A virus - immunology; Interferon-gamma - secretion; Lymphocyte Activation; Major Histocompatibility Complex; Receptors, Virus; T-Lymphocytes, Helper-Inducer - immunology; T-Lymphocytes, Regulatory - immunology
• ISSN: 0818-9641
• DOI: 10.1038/icb.1987.3

Human T cells exposed to high concentrations of influenza A virus cause specific suppression of the in vitro antibody response to the virus, but the phenomenon does not require viable T cells. In order to investigate the mechanism of this form of suppression, IL-2-dependent T cell clones of helper phenotype (CD4+, HLA-DR+, IL-2R+) were prepared with specificity for influenza A (Mem/Bel) and B (B HK) viruses and the non-crossreacting antigen purified protein derivative (PPD). When pulsed with high dose Mem/Bel virus, all three clones transferred suppression equally well to effector cultures of syngeneic or allogeneic E+ and E- cells stimulated with an immunogenic dose of the same virus. Thus, although suppression was specific at the level of expression, the induction phase was non-specific and non-major histocompatibility complex (MHC) restricted and did not involve interaction of antigen with the T cell receptor. HLA-DR, CD3 and CD8 determinants were excluded as the binding site for the virus by two-colour immunofluorescent staining and flow cytometric analysis. The concentrations of antigen required for high dose suppression inhibited antigen-specific proliferation by the clones; on the other hand, they remained partially sensitive to IL-2 and could still release gamma-interferon. These findings suggest that this phenomenon is distinct from conventional antigen-specific suppression mediated by CD8 T cells, but may play a biologically important role in regulating immune responses at least to viral antigens.