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B cells recruit dendritic cells to initiate type 2 immune responses. Lund and colleagues (p 681; News and Views by Cannons, Lu & Schwartzberg, p 630) show that dendritic cells (green) localize to the central T cell area of lymph nodes after infection with influenza virus (top). In contrast, dendritic cells accumulate outside the T cell zone in close proximity to B cell follicles (red) after infection with the nematode Heligmosomoides polygyrus (bottom). Original images by Beatriz León. Artwork by Lewis Long.
The cellular mechanism by which the cytokine TGF-β maintains the homeostasis of mature T cells and prevents the emergence of severe lethal lymphoproliferative disease has remained obscure. It is now shown that TGF-β restrains the homeostatic T cell proliferation driven by self ligands from erupting into overt autoimmunity.
The role of T cells in providing help to B cells is well established; however, the converse—that B cells provide signals to help initiate T cell–mediated immunity—is less well appreciated. New data now show B cells modulate the earliest stages of T cell activation in a T helper type 2 response.
'Elite controllers' of human immunodeficiency virus (HIV) maintain a long-term disease-free status after infection with HIV. A comparison of elite controllers and people who progress to disease after infection with HIV now suggests that clonotypic profiles of HIV-specific CD8+ T cells may underlie elite control.
Antiviral innate immunity often has deleterious effects on the course of bacterial infection. Activation of the transcription factor IRF3 induced by the recognition of double-stranded RNA by RIG-I-like receptors suppresses the Toll-like receptor–induced expression of interleukins 12 and 23 and antibacterial responses.
Notch signaling is known to modulate macrophage polarization. Hu and colleagues show that the Notch–RBP-J axis controls the expression of M1 macrophage–specific genes by promoting translation of the transcription factor IRF8.
Little is known about the regulation of the ST2L receptor for IL-33. Zhao and colleagues identify the F-box protein FBXL19 as being key to the degradation and negative regulation of ST2L.
Whether cross-interference between innate immune receptors affects the outcome of immune responses remains unclear. Taniguchi and colleagues show that RLR activation interferes with activation of the Il12b promoter induced by TLR signaling.
The pleiotropic cytokine TGF-β is involved in the generation of Treg cells and maintaining tolerance. Zhang and Bevan show that TGF-β acts specifically to block the proliferation of low-affinity T cells independently of effects on the development of Treg cells.
Tetramers of peptide and major histocompatibility complex (pMHC) are very useful for the detection of specific T cell antigen receptors; however, they have several drawbacks. Davis and colleagues describe photocrosslinkable pMHC monomers with several important advantages and use these to probe the immunological synapse.
In lymph nodes, cellular positioning can dictate the immune response. Lund and colleagues show that nematode infection triggers interactions between lymphotoxin-producing B cells and CXCR5+ dendritic cells and CD4+ T cells to initiate T helper type 2 responses.
The functional basis of elite control of HIV is still unclear. Walker and colleagues show that elite controllers are tolerant of viral escape variants and more rapidly mobilize cytotoxic granules to the immunological synapse.