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Macrophages mount complex responses to pathogens. Although several key signaling pathways have been identified, it remains unclear how they work together to provide specificity. In a recent paper, Gottschalk et al. report that differential dose–response behaviors of the NFκB and MAPK pathways allow dose-specific gene expression programs. [ABSTRACT FROM AUTHOR]

The ability of the immune system to ‘remember’ a previous encounter with antigen is the hallmark of the adaptive immune response. The signals required for CD4+ memory T cell survival are not well understood, and a recent paper lends new biochemical insights into how memory T cells might optimally be preserved through the convergence of signals from the engagement of cytokine and antigen-specific T cell receptors. [Copyright &y& Elsevier]

A major challenge for immunologists has been the development of vaccines designed to emphasize cellular immune responses. One particularly promising approach is the prime–boost strategy, which has been shown to generate high levels of T-cell memory in animal models. Recently, several papers have highlighted the power of prime–boost strategies in eliciting protective cellular immunity to a variety of pathogens and have demonstrated efficacy in humans. Coupled with recent advances in our understanding of the mechanisms underlying the generation, maintenance and recall of T-cell memory, the field is poised to make tremendous progress. This Review discusses the impact of these recent developments on the future of prime–boost vaccine strategies. [Copyright &y& Elsevier]

Immunology in recent years has taken a somewhat surprising turn, expressed by a renewed interest in innate immunity. Especially intriguing is the regulatory role exerted by the innate components on the adaptive response, with Toll receptors and complement components being the most investigated. This function has been firmly established for complement protein CR2 (CD21) as part of the BCR co-receptor CD19/CD21/CD81. New findings are now providing a broader picture of complement and its tuning of the immune response; for example, complement proteins have been implicated in the control of T-cell-mediated responses. We will review some of these data here and summarize new discoveries in areas of research on more traditional topics within the complement literature, such as complement and renal diseases, and the therapeutic use of C1-Inhibitor. We cover papers selected from studies presented at the XIX International Complement Workshop, held in Palermo in September 2002, and published within the past six months. [Copyright &y& Elsevier]

CD8+ memory T cells are critical for immunity against intracellular pathogens. Epidemiological evidence demonstrates that bystander infection can impact immune responses to co-infection or vaccination. A recent paper in Immunity demonstrates that persistent bystander inflammation can negatively impact CD8+ T cell effector to memory transition and protection from subsequent infection. [ABSTRACT FROM AUTHOR]

Until recently, two key members of the innate immune response to Gram negative bacteria, bactericidal permeability-increasing protein (BPI) and lipopolysaccharide (LPS)-binding protein (LBP), have been considered to be members of a small family of lipid-binding proteins that also contains cholesteryl ester transfer protein (CETP) and phospholipid transfer protein (PLTP). A recent paper has characterised three related proteins that are expressed in the mouth, nose and upper airways. Taken together with other recent data, it is clear that a large family of such proteins exists and these additional members might also function in the innate immune response. [Copyright &y& Elsevier]

Vitamin A plays pleiotropic roles in the immune system. A recent eLife paper by Hooper and colleagues shows that hepatic and intestinal serum amyloid A proteins, which are induced in response to infection, can transport vitamin A metabolites to tissues and thus impact immune responses both locally and systemically. [ABSTRACT FROM AUTHOR]

Immune suppression by Treg cells must be overcome to mount robust and effective anti-pathogen immune responses. A new paper in Immunity from Medzhitov and colleagues shows that IL-1-dependent activation of MyD88 promotes the development of Th1 cells by rendering them impervious to Treg cell-mediated inhibition. [ABSTRACT FROM AUTHOR]