Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
T cells become nonresponsive, or anergic, in certain Ca2+-dependent conditions. Rao and colleagues (p 255; News and Views by Ben-Neriah, p 238) find that anergy proceeds in a stepwise way that targets the degradation of key signaling components. Ultimately, the outer ring of LFA-1 adhesion proteins (red) in the immune synapse starts to dissolve away from the inner T cell receptors (green). Original photo by Rajat Varma; artwork is Lewis Long.
Eliciting broadly neutralizing antibodies to human immunodeficiency virus could bring closer the goal of a successful AIDS vaccine. Here the International AIDS Vaccine Initiative Neutralizing Antibody Consortium discusses current approaches to overcome the problems faced.
Natural killer cells are kept in check by their inhibitory receptors. Data now indicate that these receptors can bind ligands that are next to them on the same cell surface, with unexpected functional consequences.
Anergy induction initiates a transcription program involving the upregulation of several ubiquitin ligases (E3s). New data show how these E3s contribute to the establishment of anergy.
When acetyl or methyl groups are added to histones, chromatin structure and gene expression are altered. The methyltransferase G9a can target the specific silencing of IFNB gene expression and blocking of V(D)J recombination.
Viral TH1 responses can positively regulate TH2 responses in a mouse model of allergen-induced lung inflammation. This helps explain why respiratory viral infections can exacerbate allergic TH2-type diseases.