Immune regulation

A neuronal receptor, neuropilin-1, is essential for the initiation of the primary immune response.Tordjman, R. et al. Nature Immunol. 3, 477–482 (2002)

Neuropilin-1 is a transmembrane receptor that is involved in axon guidance. This study shows that neuropilin-1 is expressed by dendritic cells (DCs) and T cells, and mediates a homophilic interaction between these two cell types. Preincubation of either T cells or DCs with blocking neuropilin-1-specific antibodies blocked T-cell proliferation, which indicates that the expression of neuropilin-1 on both cell types is important for the initiation of an immune response.

T-cell signalling

c-Jun NH2-terminal kinase (JNK)1 and JNK2 have distinct roles in CD8+ T-cell activation.Conze, D. et al. J. Exp. Med. 195, 811–823 (2002)

c-Jun NH2-terminal kinase (JNK)1 and JNK2 signaling pathways have divergent roles in CD8+ T-cell-mediated antiviral immunity.

Arbour, N. et al. J. Exp. Med. 195, 801–810 (2002)

The c-Jun NH2-terminal kinase (JNK) signalling pathway is induced by cytokine signalling and stress stimuli, and it has been implicated in the control of T-cell proliferation and differentiation. These studies used Jnk1−/− and Jnk2−/− mice to investigate the physiological role of these kinases in CD8+ T-cell responses. Conze et al. showed that Jnk2 deficiency resulted in increased interleukin-2 (IL-2) production and the increased proliferation of CD8+ T cells. By contrast, Jnk1−/− CD8+ T-cell populations were unable to expand after antigen stimulation, even in the presence of endogenous IL-2. Arbour et al. investigated the role of JNKs in antiviral T-cell immunity. After viral infection, virus-specific CD8+ T-cell expansion was reduced in Jnk1−/− mice compared with wildtype mice, but was increased in Jnk2−/− mice. Therefore, Jnk1 and Jnk2 have distinct roles in CD8+ T-cell responses.

Isotype switching

The AID enzyme induces class switch recombination in fibroblasts.Okazaki, I. M. et al. Nature 416, 340–345 (2002)

The putative RNA-editing enzyme AID (activation-induced cytidine deaminase) is expressed only in activated B cells and is essential for class-switch recombination (CSR). To examine the molecular basis of CSR, an artificial substrate was developed that allows the detection of CSR by the expression of a green-fluorescent-protein-based marker. Using this substrate, the authors found that the ectopic expression of AID in non-B cells, such as fibroblast and T-cell lines, was sufficient to induce CSR, providing that the substrate was actively transcribed. This indicates that AID is the only B-cell-specific factor that is required for CSR at an active locus.