Fachbereich Veterinärmedizin



    IL-10 dependent suppression of type 1, type 2 and type 17 cytokines in active pulmonary tuberculosis (2013)

    Zeitschriftenartikel / wissenschaftlicher Beitrag
    Kumar, Nathella Pavan
    Gopinath, Venugopal (WE 6)
    Sridhar, Rathinam
    Hanna, Luke E
    Banurekha, Vaithilingam V
    Jawahar, Mohideen S
    Nutman, Thomas B
    Babu, Subash
    PLoS one; 8(3) — S. e59572
    ISSN: 1932-6203
    DOI: 10.1371/journal.pone.0059572
    Pubmed: 23544075
    Institut für Immunologie

    Robert-von-Ostertag-Str. 7-13
    Gebäude 35
    14163 Berlin
    +49 30 838 51834

    Abstract / Zusammenfassung

    Although Type 1 cytokine responses are considered protective in pulmonary tuberculosis (PTB), their role as well as those of Type 2, 17 and immunoregulatory cytokines in tuberculous lymphadenitis (TBL) and latent tuberculosis (LTB) have not been well studied.

    To identify cytokine responses associated with pulmonary tuberculosis (TB), TB lymphadenitits and latent TB, we examined mycobacterial antigen-specific immune responses of PTB, TBL and LTB individuals. More specifically, we examined ESAT-6 and CFP-10 induced Type 1, Type 2 and Type 17 cytokine production and their regulation using multiplex ELISA.

    PTB individuals exhibited a significantly lower baseline as well as antigen-specific production of Type 1 (IFNγ, TNFα and IL-2); Type 2 (IL-4) and Type 17 (IL-17A and IL-17F) cytokines in comparison to both TBL and LTB individuals. TBL individuals exhibited significantly lower antigen-specific IFNγ responses alone in comparison to LTB individuals. Although, IL-10 levels were not significantly higher, neutralization of IL-10 during antigen stimulation resulted in significantly enhanced production of IFNγ, IL-4 and IL-17A in PTB individuals, indicating that IL-10 mediates (at least partially) the suppression of cytokine responses in PTB.

    Pulmonary TB is characterized by an IL-10 dependent antigen-specific suppression of Type 1, Type 2 and Type 17 cytokines, reflecting an important association of these cytokines in the pathogenesis of active TB.