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In a recent paper, Schriek et al. show that, in a complement-dependent reaction, marginal zone B cells (MZBs) steal MHC class II (MHCII) from dendritic cells (DCs). Activation of T cells by stolen MHCII complexes potentially allows MZBs to augment or regulate T cell activation in ways that are distinct from DCs. [ABSTRACT FROM AUTHOR]

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]

The TCL1 (T-cell leukemia 1) protooncogene is highly expressed in many human B-cell leukemias and two recent papers show that TCL1 overexpression causes rapid development of B-cell lymphomas in mice. Other recent work showing that the TCL1 protein enhances the activation of the pro-survival kinase Akt has revealed a potential mechanism underlying the development of B-cell leukemias and raised new questions about the regulation of Akt. [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]

The entry of exogenous antigen into the MHC class I-restricted crosspresentation pathway can contribute to CD8+ T cell tolerance and immunity, in particular to peripheral self-antigens or selected viruses and bacteria showing restricted tissue tropism. Dendritic cells are the key crosspresenting cells and, as such, they are thought to carry specialized machinery dedicated to this purpose. Two recent papers describe intracellular components tailored to the dendritic cell crosspresentation pathway. [Copyright &y& Elsevier]

CD8 T-cell immunity is thought to require helper activity derived from CD4 T cells. Nevertheless, under some circumstances, effective CD8-dependent T-cell responses occur in vivo without CD4 T-cell help. Several recent papers help to explain this paradox and lead to a refined view concerning the role of T helper cells and interleukin-2 receptor signaling in the production of cytotoxic T lymphocytes. [ABSTRACT FROM AUTHOR]

Occasionally, the discovery of a new molecule sheds light on an entire biological system. A good example is the discovery of the tumor necrosis factor (TNF)-related molecule, B-cell-activating factor belonging to the TNF family (BAFF), known also as BLyS, TALL-1, zTNF4 or THANK. A flurry of papers from several groups, describing results from transgenic and knockout mice, animal models and human studies, has shown that BAFF is a crucial molecule involved in B-cell maturation and the development of autoimmunity. Several recent reports add to this exciting story and illustrate some of the formative stages of B-cell maturation and tolerance. [Copyright &y& Elsevier]

Regulatory T cells are crucial for preventing autoimmunity, but how their function is restrained to allow optimal effector T cells responses in appropriate contexts is unclear. In a recent paper in the Journal of Experimental Medicine, Campbell and colleagues demonstrate that virus-induced type I interferon acts directly on Treg cells to allow for functional antiviral T cell responses. [ABSTRACT FROM AUTHOR]

Human genetic and environmental factors underlie susceptibility to the T cell-mediated autoimmune disease, multiple sclerosis (MS). How the environment influences the pathogenesis of MS has been difficult to parse. A recent paper in Cell shows that environmental antigens that activate myelin-specific T cells can be identified with unprecedented accuracy. [Copyright &y& Elsevier]

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]

A recent paper on immunity and tolerance to antigenic determinants on antibody variable-regions (idiotypes) brings back to light the potential of idiotypic interactions among antibodies, B cells and T cells in the regulation of specific immune activities. The functional significance of idiotypic regulation has been established in a variety of systems, both concerning the establishment of ‘pre-immune’ diversity repertoires as well as the clonal regulation of immune responses to foreign and self-antigens. Also, recently the requirement for ‘dominant’ regulatory mechanisms in natural tolerance has received increasing support. It might thus be fruitful to evaluate the possibility that an idiotypic network has a fundamental role in the operation of the regulatory T cells that establish and maintain self-tolerance. [Copyright &y& Elsevier]