Recruitment of A20 by the C-terminal domain of NEMO suppresses NF-κB activation and autoinflammatory disease.

Receptor-induced NF-κB activation is controlled by NEMO, the NF-κB essential modulator. Hypomorphic NEMO mutations result in X-linked ectodermal dysplasia with anhidrosis and immunodeficiency, also referred to as NEMO syndrome. Here we describe a distinct group of patients with NEMO C-terminal deletion (ΔCT-NEMO) mutations.

HIV-1 transmission and cytokine-induced expression of DC-SIGN in human monocyte-derived macrophages.

Dendritic cell-specific intercellular adhesion molecule-3-grabbing nonintegrin (DC-SIGN) has been described as an attachment molecule for human immunodeficiency virus type 1 (HIV-1) with the potential to mediate its transmission. We examined DC-SIGN expression in monocyte-derived macrophages (MDM) and its role in viral transmission when MDM were exposed to interleukin (IL)-13, IL-4, or interferon-gamma (IFN-gamma). We show that IL-13 and IL-4 increase transcripts, total protein, and cell-surface expression of DC-SIGN in all MDM tested, IFN-gamma results ranged from no change to up-regulation of surface expression, and message and total protein were, respectively, induced in all and 86% of donors tested.

Simian immunodeficiency virus encephalitis: analysis of envelope sequences from individual brain multinucleated giant cells and tissue samples.

Simian immunodeficiency virus (SIV)-infected macaques develop an encephalitis (SIVE) that is pathologically virtually indistinguishable from that associated with HIV infection, with multinucleated giant cells (MNGCs) being the principal histopathological manifestation. To dissect SIV variants responsible for MNGC development, we examined the relationships between env sequences transcribed in individual MNGCs and those from genomic DNA of brain and spleen tissues. The brain-specific variant found in all brain clones was dominant among the clones from MNGCs, suggesting a role in the formation of giant cells.