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Type I, II, and III Interferons: Regulating Immunity to Mycobacterium tuberculosis Infection

  • Maja TravarEmail author
  • Miroslav Petkovic
  • Antonija Verhaz
Review

Abstract

Interferons (IFNs) are cytokines released by host cells in response to the presence of pathogens or tumor cells. The aim of this review was to present the previously known and new findings about the role of interferons type I and II, and recently discovered type III in Mycobacterium tuberculosis (M. tuberculosis) infection control. Infection of various cell types with M. tuberculosis induce both IFN-α and IFN-β synthesis. The majority of the studies support the findings that IFN type I actually promotes infection with M. tuberculosis. It has been well establish that IFN-γ has protective function against M. tuberculosis and the other mycobacteria and that the primary source of this cytokine are CD4+ and CD8+ T cells. Recently, it has been shown that also the innate lymphocytes, γδ T cells, natural killer (NK) T cells, and NK cells can also be the source of IFN-γ in response to mycobacterial infection. Several studies have shown that CD4+ T cells protect mice against M. tuberculosis independently of IFN-γ. The balance between IFN-γ and different cytokines such as IL-10 and other Th2 cell cytokines is likely to influence disease outcome. Type I IFN appears to be detrimental through at least three separate, but overlapping, type I IFN-mediated mechanisms: induction of excessive apoptosis, specific suppression of Th1 and IFN-γ responses, and dampening of the immune response by strong IL-10 induction. Recently it has been found that M. tuberculosis infection in A549 lung epithelial cells stimulate up-regulation of IFN-λ genes in vitro. IFN-λs also have a role in modulation of Th1/Th2 response. IFN-λs are not essential for M. tuberculosis infection control, but can give some contribution in immune response to this pathogen.

Keywords

Interferon Interferon lambda Mycobacterium tuberculosis 

Notes

Compliance with ethical standards

Conflict of interest

None to declare.

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Copyright information

© L. Hirszfeld Institute of Immunology and Experimental Therapy, Wroclaw, Poland 2015

Authors and Affiliations

  • Maja Travar
    • 1
    • 2
    Email author
  • Miroslav Petkovic
    • 2
  • Antonija Verhaz
    • 3
  1. 1.Department of MicrobiologyUniversity Hospital Clinical Centre Banja LukaBanja LukaRepublic of Srpska, Bosnia and Herzegovina
  2. 2.Department of Microbiology and Immunology, Faculty of MedicineBanja Luka UniversityBanja LukaRepublic of Srpska, Bosnia and Herzegovina
  3. 3.Clinic for Infectious DiseasesUniversity Hospital Clinical Centre Banja LukaBanja LukaRepublic of Srpska, Bosnia and Herzegovina

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