Interferon and tumor necrosis factor production by peripheral blood leukocytes of patients with infectious

T Kamińska1, M Kandefer-Szerszeń, A Szuster-Ciesielska

  • 1Department of Virology and Immunology, Maria Curie-Skłodowska University, Lublin, Poland.

Insights

Infectious mononucleosis (IM) patients show altered cytokine production. While interferon (IFN) levels decrease during acute IM, tumor necrosis factor (TNF) increases, suggesting a complex immune response.

Area of Science:

  • Immunology
  • Virology
  • Infectious Diseases

Background:

  • Infectious mononucleosis (IM) is a viral illness characterized by immune system dysregulation.
  • Cytokines like Interferon-alpha (IFN-alpha) and Tumor Necrosis Factor-alpha (TNF-alpha) play crucial roles in immune responses to viral infections.

Purpose of the Study:

  • To investigate the levels and production capacity of IFN-alpha and TNF-alpha in patients with infectious mononucleosis during acute and convalescent phases.
  • To compare the in vitro cytokine response of leukocytes from IM patients with healthy controls.

Main Methods:

  • Blood samples were collected from 29 IM patients during acute and convalescent phases.
  • Serum cytokine levels (IFN-alpha, TNF-alpha) were measured.
  • Whole blood assays were performed using various inducers (Newcastle disease virus, phytohemagglutinin, concanavalin A, lipopolysaccharide) to assess in vitro cytokine production by leukocytes.

Main Results:

  • IFN-alpha and TNF-alpha were detected in sera during both acute and convalescent IM phases.
  • IFN titers were higher in the acute phase, while TNF titers peaked in the convalescent phase.
  • Leukocytes from acutely ill IM patients showed reduced in vitro IFN production in response to NDV, PHA, and ConA, but increased TNF production in response to LPS compared to convalescent patients and controls.

Conclusions:

  • Leukocyte dysfunction in cytokine production is evident during acute infectious mononucleosis.
  • The observed increase in TNF production during the acute phase warrants further investigation into its role in IM pathogenesis, potentially similar to its role in HIV infection.

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