Efficient activation of T cells by human monocyte-derived dendritic cells (HMDCs) pulsed with Coxiella burnetii outer membrane protein Com1 but not by HspB-pulsed HMDCs

The recombinant proteins Com1 and HspB were applied to pulse human monocyte-derived dendritic cells (HMDCs), and the pulsed HMDCs were used to stimulate isogenic T cells. Com1-pulsed HMDCs expressed substantially higher levels of surface molecules (CD83, CD40, CD80, CD86, CD54, and CD58) and a higher level of interleukin-12 than HspB-pulsed HMDCs. Moreover, Com1-pulsed HMDCs induced high-level proliferation and activation of CD4+ and CD8+ cells, which expressed high levels of T-cell activation marker CD69 and inflammatory cytokines IFN-γ and TNF-α. In contrast, HspB-pulsed HMDCs were unable to induce efficient T-cell proliferation and activation.Our results demonstrate that Com1-pulsed HMDCs are able to induce efficient T-cell proliferation and drive T cells toward Th1 and Tc1 polarization; however, HspB-pulsed HMDCs are unable to do so. Unlike HspB, Com1 is a protective antigen, which was demonstrated by the adoptive transfer of Com1-pulsed bone marrow dendritic cells into naive BALB/c mice.Dendritic cells (DCs) are potent antigen-presenting cells (APCs) that bridge the innate and adaptive immune responses through direct pathogen neutralization, cytokine production, and T-cell activation [1]. Activated DCs express major histocompatibility complex (MHC) I and MHC II molecules and T-cell costimulatory molecules, which possess the unique ability to activate naive T cells [2,3]. Immature DCs (iDCs) reside in the peripheral epithelial tissues, where they serve as sentinels against invading microorganisms [4]. Contact with a pathogen typically elicits stimulation of iDCs via pattern-recognition receptors, such as the toll-like receptor (TLR), and subsequent conversion of iDCs to mature DCs (mDCs) [5,6]. mDCs exhibit a reduction in phagocytic ability and an increase in surface expression of MHC II and costimulatory molecules, and they switch in chemokine receptor expression, which results in mDC migration to the local lymph nodes to induce adaptive immunity [2,7,8].Coxiel