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Plasmacytoid dendritic cells selectively express Toll-like receptors 7 and 9 and respond to virus infection by triggering massive interferon production, a pathway regulated by osteopontin expressed in plasmacytoid dendritic cells.
The adaptor protein MyD88 is involved in interleukin 1 receptor and Toll-like receptor signaling. Unexpectedly, new evidence shows that MyD88 also participates in interferon-γ-induced cellular responses.
Ikaros regulatory proteins are essential for proper lymphoid cell development. Several new functions for Ikaros have been defined by surrogate marker expression in early hematopoietic progenitor populations.
Deubiquitinating enzymes remove polyubiquitin chains from and alter the fate of specific target proteins. The CYLD deubiquitinating enzyme regulates proximal T cell receptor signaling in thymocytes by selectively binding to and deubiquitinating the active form of the kinase Lck.
Precursors of specialized skin dendritic cells called Langerhans cells are derived from specific bone marrow–derived monocyte precursors that migrate to the skin and differentiate into these important immune surveillance cells.
Functional and phenotypic distinctions characterize B-1 cells versus B-2 cells. The identification of adult bone marrow cells that give rise exclusively to B-1 B cells support earlier ideas regarding the existence of dedicated B-1 progenitors.
It is unclear whether T cell exhaustion is reversible. A recent Nature paper shows that in vivo blockade of the inhibitory molecule PD-1 can restore the function of exhausted CD8+ T cells during chronic viral infection.
Lentiviral Nef protein has many functions in the evasion of host immune defenses. Another 'chink' in the host immune 'armor' has now been exposed by Nef's ability to inhibit immunoglobulin class switching.
The chemokine receptor CCR2 was believed to 'summon' infiltrating CCR2+ monocytes into the spleen. Instead, CCR2 seems to be important for 'release' of these cells from bone marrow niches.
Substitutions in CD8+ T cell epitopes in viral proteins can alter the complex interaction between viruses and host immunity. Reduced viral fitness and recognition of altered and subdominant epitopes are possible outcomes.
Suppressor of cytokine signaling 1 has been linked to the negative regulation of Toll-like receptor signaling. The mechanism for this seems to be suppressor of cytokine signaling 1–mediated degradation of the adaptor Mal, which is required for Toll-like receptor signaling.
Naive CD8+ T cells can be activated via dendritic cell 'cross-priming' of antigens obtained exogenously. Dendritic cells cannot cross-prime, however, after systemic activation in vivo, potentially contributing to immunosuppression associated with severe infections.
'Forward' genetic approaches for elucidating function can lead to unexpected findings. A single missense mutation is found to disrupt both antigen presentation and nucleic acid Toll-like receptor signaling, two processes involving endocytic pathways.
CD8+ T cell recognition of peptides presented by major histocompatibility complex class I molecules is essential for effective antiviral and antitumor immune responses. How the repertoire of peptides is selected, shaped and presented is becoming increasingly clear.
How regulatory T cells dampen T cell responses in vivo remains unclear. Direct visualization of regulatory T cell activity in an autoimmune setting provides exciting new insights into regulatory T cell–mediated suppression.
The thymus is considered the source of mature lymphocytes and is not thought to produce progenitors with the capacity to develop into unconventional T cells in the periphery. That view requires revision.
Discrimination between self and bacterial DNA has been attributed in part to differential modification of prokaryotic and eukaryotic DNA. However, cellular localization of innate DNA receptors may be even more important.
The function of TRAF3, a member of the family of tumor necrosis factor receptor–associated factors, has remained an enigma. Two recent Nature papers now show that TRAF3 regulates interferon and interleukin 10 production.
