Dominance of CD86, Transforming Growth Factor–β1, and Interleukin‐10 inMycobacterium tuberculosisSecretory Antigen–Activated Dendritic Cells Regulates T Helper 1 Responses to Mycobacterial Antigens | Zendy

Mumtaz Yaseen Balkhi | Zendy; Aprajita Sinha | Zendy; Krishnamurthy Natarajan | Zendy

Open Access

Dominance of CD86, Transforming Growth Factor–β1, and Interleukin‐10 inMycobacterium tuberculosisSecretory Antigen–Activated Dendritic Cells Regulates T Helper 1 Responses to Mycobacterial Antigens

Author(s) -

Mumtaz Yaseen Balkhi,

Aprajita Sinha,

Krishnamurthy Natarajan

Publication year - 2004

Publication title -

the journal of infectious diseases

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.69

H-Index - 252

eISSN - 1537-6613

pISSN - 0022-1899

DOI - 10.1086/383328

Subject(s) - cd86 , antigen , dendritic cell , proinflammatory cytokine , immunology , interferon gamma , interleukin 4 , biology , cytokine , antigen presenting cell , mycobacterium tuberculosis , interleukin 10 , t cell , microbiology and biotechnology , chemistry , immune system , tuberculosis , medicine , inflammation , pathology

We report that stimulation of Mycobacterium tuberculosis (M. tuberculosis) secretory antigen (MTSA)-differentiated dendritic cells (DCs) and MTSA-matured DCs with M. tuberculosis cell extract (CE) down-regulated proinflammatory responses to CE-primed T (CE-T) cells by increasing surface expression of CD86 after CE stimulation. CE stimulation also decreased interleukin (IL)-12p40 and interferon (IFN)- gamma levels and increased IL-10 and transforming growth factor- beta 1 (TGF- beta 1) levels from these DCs. Blocking either CD86, IL-10, or TGF- beta with monoclonal antibodies before CE stimulation restored the attenuated T helper 1 (Th1) responses of CE-T cells. Conversely, treatment of these DCs with IL-12p70 and/or IFN- gamma completely restored Th1 responses from CE-T cells. These results indicate that M. tuberculosis secretory antigens down-regulate proinflammatory Th1 responses to mycobacteria by differentially modulating the cytokine profiles and surface densities of costimulatory molecules on DCs. Of importance, this down-regulation is independent of the maturation status of MTSA-activated DCs and can be rescued after treatment of DCs with IFN- gamma or IL-12.

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