Abstract
BackgroundControl of Mycobacterium tuberculosis (Mtb) infection requires CD4+ T-cell responses and major histocompatibility complex class II (MHC II) presentation of Mtb antigens (Ags). Dendritic cells (DCs) are the most potent of the Ag-presenting cells and are central to the initiation of T-cell immune responses. Much research has indicated that DCs play an important role in anti-mycobacterial immune responses at early infection time points, but the kinetics of Ag presentation by these cells during these events are incompletely understood.ResultsIn the present study, we evaluated in vivo dynamics of early Ag presentation by murine lymph-node (LN) DCs in response to Mycobacterium bovis bacillus Calmette–Guérin (BCG) Ag85A protein. Results showed that the early Ag-presenting activity of murine DCs induced by M. bovis BCG Ag85A protein in vivo was transient, appearing at 4 h and being barely detectable at 72 h. The transcription levels of CIITA, MHC II and the expression of MHC II molecule on the cell surface increased following BCG infection. Moreover, BCG was found to survive within the inguinal LN DC pool, representing a continuing source of mycobacterial Ag85A protein, with which LN DCs formed Ag85A peptide-MHCII complexes in vivo.ConclusionsOur results demonstrate that a decrease in Ag85A peptide production as a result of the inhibition of Ag processing to is largely responsible for the short duration of Ag presentation by LN DCs during BCG infection in vivo.
Highlights
Control of Mycobacterium tuberculosis (Mtb) infection requires CD4+ T-cell responses and major histocompatibility complex class Major histocompatibility complex class II (II) (MHC II) presentation of Mtb antigens (Ags)
We evaluated the in vivo dynamics of early Ag presentation by murine inguinal LN Dendritic cell (DC) in response to M. bovis bacillus Calmette–Guérin (BCG)
The results showed that the early Ag-presenting activity of murine DCs induced by M. bovis BCG Ag85A protein in vivo was transient and that the inhibition of Ag processing due to the decreased production of Ag85A peptide is the primary reason for the rapid loss of Ag85A peptide-major histocompatibility complex class II (MHC II) complexes
Summary
Control of Mycobacterium tuberculosis (Mtb) infection requires CD4+ T-cell responses and major histocompatibility complex class II (MHC II) presentation of Mtb antigens (Ags). Dendritic cells (DCs) are the most potent of the Ag-presenting cells and are central to the initiation of T-cell immune responses. Much research has indicated that DCs play an important role in anti-mycobacterial immune responses at early infection time points, but the kinetics of Ag presentation by these cells during these events are incompletely understood. Tuberculosis (TB), caused by infection with Mycobacterium tuberculosis (Mtb), remains a major disease worldwide and is the leading infectious disease in terms of mortality, being responsible for an estimated 1.3 million deaths globally in 2016. Dendritic cells (DCs) represent the bridge between the innate and adaptive immune responses and strengthen the cellular immune response against mycobacterial infections [6, 7].
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