Fc gamma receptor I (CD64)-negative human monocytes are potent accessory cells in viral antigen-induced T cell activation and exhibit high IFN-alpha-producing capacity.
Blood monocytes represent a heterogeneous cell population with respect to phenotype and function. We have previously described that a minor subset of Fc gamma receptor I-negative (CD64-) monocytes, comprising < 10% of all monocytes, exhibits a significantly higher accessory capacity in allogeneic or purified protein derivative (PPD) of tuberculin-induced T cell activation than the majority of CD64-expressing (CD64+) monocytes. CD64- monocytes were also found to represent the major source of Newcastle disease virus (NDV)-induced interferon (IFN)-alpha within human monocytes. In the present study we demonstrate that CD64- monocytes are also the main producers of IFN-alpha in response to Herpes simplex virus type 1 (HSV-1) or influenza (type A) antigens. The virus-induced IFN-alpha release by monocytes, but mainly that by CD64- monocytes, can be further increased by co-culture with autologous T cells, which alone do not produce significant amounts of IFN-alpha in response to virus. In addition, CD64- and CD64+ monocytes also differ in their accessory capacity in virus-induced T cell responses. CD64- monocytes exposed to influenza antigens induced higher IFN-gamma release and proliferation by the responding autologous T cells than virus-exposed CD64+ monocytes. In virus-stimulated monocyte/T cell co-cultures, CD64- monocytes also induced larger size cell clusters than CD64+ monocytes, indicating direct cell-to-cell interaction with a higher number of T cells, which represent the main component of these clusters.
Grage-Griebenow
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Forschungszentrum Borstel, Department of Immunology and Cell Biology, Federal Republic of Germany.
Flad
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HD
Ernst
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D000938:Antigen-Presenting Cells / Q000276:immunology / Q000378:metabolism / Q000502:physiology*; D000956:Antigens, Viral / Q000276:immunology / Q000494:pharmacology*; D002450:Cell Communication / Q000502:physiology; D018259:Herpesvirus 1, Human / Q000276:immunology; D006801:Humans; D009980:Influenza A virus / Q000276:immunology; D009981:Influenza B virus / Q000276:immunology; D016898:Interferon-alpha / Q000096:biosynthesis* / Q000378:metabolism; D007371:Interferon-gamma / Q000378:metabolism; D007963:Leukocytes, Mononuclear / Q000276:immunology / Q000378:metabolism / Q000502:physiology*; D008213:Lymphocyte Activation / Q000502:physiology*; D017452:Receptors, IgG / Q000502:physiology*; D013601:T-Lymphocytes / Q000502:physiology*
D000956:Antigens, Viral; D016898:Interferon-alpha; D017452:Receptors, IgG; D007371:Interferon-gamma