Participation of CD1 Molecules in the Presentation of Bacterial Protein Antigens in Humans

Abstract

Human CD1 molecules, expressed on the surface of professional antigen-presenting cells (including dendritic cells, Langerhans' cells, B cells and activated monocytes) are structurally homologous to major histocompatibility complex (MHC) class I and class II molecules. CD1b and CD1c have been shown to present nonpeptide bacterial antigens to T cells. We hypothesized that CD1 molecules may also be involved in the presentation of bacterial protein antigens. Human peripheral blood mononuclear cells (PBMC) were exposed to two medically important proteins, tetanus toxoid (TT) and puri®ed protein derivative (PPD), with and without murine monoclonal antibodies (MoAbs) speci®c for CD1a, CD1b and CD1c. All the MoAbs substantially inhibited the proliferative responses of PBMC to TT and PPD. Simultaneous interaction of CD1 and MHC class II molecules was even more inhibitory to these antigen-speci®c proliferative responses. In contrast, neither mixed lymphocyte reaction nor superantigen and mitogenic responses were affected by CD1-speci®c antibodies, indicating a certain restriction pattern in antigen presentation. Our ®ndings suggest that, besides MHC class I and II molecules, there is a family of nonpolymorphic cell surface molecules that is able to present certain bacterial protein antigens to T cells.

Characterization of the interaction of staphylococcal enterotoxin B with CD1d expressed in human renal proximal tubule epithelial cells

“…The essential role of renal CD1d in SEB-associated pathogenesis was further validated with a fluorescence-based assay demonstrating the sequential inhibition of CD1d and preventing its binding to SEB (Figure 5 ). In agreement, multiple studies observed diminished host defense as a result of the targeted CD1d deficiency [ 37 , 40 , 59 , 60 ]. It was, however, beyond the scope of the present study to suggest putative SEB-induced toxemia through CD1d-independent routes.…”

“…The involvement of CD1d in pathogenesis has been investigated in the past, primarily focused on the lymphoid cells [ 37 - 41 ], while the knowledge gap exists in comprehending the CD1d-mediated pathogenesis in kidney cells and its role in the late stage of pathogenesis. To bridge the knowledge gap, our study sought to understand the renal response to SEB shock, focusing on the interaction of SEB with CD1d in RPTECs.…”

Specific lytic activity against mycobacterial antigens is inversely correlated with the severity of tuberculosis

“…In order to analyse the nature of ex vivo effector cells, 1 × 10 6 PBMC were incubated with 10 µ g/ml of anti‐CD56 (Leu‐19, Becton Dickinson), anti‐CD16 (clone 3G8, IgG1, Immunotech) [26] or 1 µ g/ml of anti‐TCR γδ (Pan γ/δ , clone IMM 510, Immunotech) MoAb. Target cells were incubated with 10 µ g/ml of anticlass‐I MHC (anti‐HLA‐ABC, IgG2 κ (mouse), clone B9·12·1, Immunotech), anticlass‐II MHC (anti‐HLA‐DR, IgG2a, clone L243, Becton Dickinson) or anti‐CD1b (anti‐CD1b, IgG2a, clone 4.A7·6, Immunotech) [27] MoAb. After 1 h‐incubation at 37°C, effector and target cells were washed twice and used in the cytotoxic assay.…”

CD1a in human cancers: a new role for an old molecule

“…Presentation of protein antigens by CD1 molecules, such as tetanus toxoid (TT), has also been reported [8]. Specific upregulation of CD1a, CD1b and CD1c on circulating monocytes in vitro as well as in vivo by TT has also been shown, suggesting a role for CD1 molecules in the immune response to TT [9].…”