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Volume 9 Issue 4, April 2008

The bone marrow contains specialized niches that support hematopoiesis. Jung and colleagues (p 388) identify a new dendritic cell subset that provides survival factors for mature B cells residing in the bone marrow. The original image shows perivascular dendritic cells (green) and blood vessels (red) in mouse skull bone marrow. Image by Anita Sapoznikov & Vyacheslav Kalchenko. Artwork by Lewis Long.

Volume 9 Issue 4

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Editorial

  • New accession codes and links pack even more information into Nature Immunology research articles

    Editorial

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  • Hearing about past and present issues in the world community of immunology can enrich all of us.

    Editorial
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Obituary

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Essay

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Commentary

  • Over the past decade immunological research in China has developed rapidly. This commentary describes the history, summarizes the present research funding system, institutions and representative work, and discusses the future of immunological research in China.

    • Xuetao Cao
    Commentary
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News & Views

  • TLR4 somehow manages to activate both MyD88- and TRIF-dependent signaling. According to Medzhitov and colleagues, TLR4 engages MyD88 and TRIF sequentially at the cell surface and in endosomes, respectively, thereby providing access to distinct pools of signaling proteins.

    • Colin Watts
    News & Views

  • The bone marrow contains specialized microenvironments that maintain blood cells and supply the requisite factors for their development. Newly identified bone marrow–resident dendritic cells create unique niches for mature B cells.

    • Takashi Nagasawa
    News & Views

  • The homing of lymphocytes to secondary lymphoid organs occurs at specialized blood vessels, the high endothelial venules. Autotaxin, a phospholipid-producing enzyme secreted by high endothelial venule endothelium, is a new participant found to facilitate the entry of lymphocytes into secondary lymphoid organs.

    • Dietmar Vestweber
    • Martin K Wild
    News & Views

  • Activation of the transcription factor NF-κB by Toll-like receptors must be controlled to avoid excessive inflammation. The tripartite-motif protein family member TRIM30α has now been shown to mediate a negative regulatory feedback mechanism curtailing such responses.

    • Andrew G Bowie
    News & Views
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