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The mechanisms governing natural killer cell development are not well understood. Activation of the tyrosine kinase receptors Tyro3, Axl and Mer on pre–natural killer cells by stromal cell–produced ligands now seems to be critical.
Cognate antigen triggers B cells to undergo antibody maturation and terminal differentiation into antibody-secreting plasma cells. The transcription factor IRF4, which is essential for early B cell development, is also influential at these later stages of B cell development and function.
The body responds to infections by rapidly 'ramping up' production of innate immune cells. New findings indicate that distinct transcription factors regulate 'basal' and 'emergency' leukocyte production.
Toll 2006, Recent Advances in Pattern Recognition, held in Salvador, Brazil, 4–7 March 2006, was both comprehensive and cutting edge, covering topics ranging from molecular recognition and signaling to new therapies in the clinic.
Thymic stromal lymphopoietin, a four helix–bundle cytokine, is expressed mainly by barrier epithelial cells and is a potent activator of several cell types, particularly myeloid dendritic cells. TSLP influences the outcome of interactions between dendritic cells and CD4+ thymocytes and T cells in many situations, such as the regulation of the positive selection of regulatory T cells, maintenance of peripheral CD4+ T cell homeostasis and induction of CD4+ T cell–mediated allergic inflammation.
Dendritic cells initiate immune responses but also influence regulatory T cell activity and homeostasis. Functional outcomes of dendritic cell–T cell interactions depend on the immunological context of their encounter.
Immune responses to bacterial infection occur by host cell detection of bacterial components. Monomeric flagellin can be elicited directly by host cells and then are 'sensed' by the cytosolic protein Ipaf.
The integrated stress response is a complex signaling pathway that regulates myriad cell processes, including protein translation, depending on the stress conditions. Primed CD4+ T helper cells may use this response system to optimize cytokine expression.
To prevent RNA virus–dependent tissue damage caused by interferon-regulatory factor 3 (IRF3)–induced type I interferons, proteasome-dependent destruction of IRF3 is orchestrated by the cytoplasmic prolyl isomerase Pin1.
T helper cells that produce interleukin 17 can promote a range of immune-mediated inflammatory diseases. Papers in Nature and Immunity suggest transforming growth factor-β promotes the differentiation of these pathogenic cells.
The resolution of immune responses typically leaves a population of memory T cells to respond to subsequent infection. The generation of 'memory-like' T cells can also occur during homeostatic proliferation, but are they 'true' memory cells?
NKp46, an activating receptor expressed on natural killer cells, protects from lethal influenza virus infection. Contrary to prevailing views, involvement of NKp46 in tumor immunity is uncertain.
B lymphocyte–induced maturation protein 1 (Blimp-1) is known as a 'master regulator' of plasma cell differentiation. New findings suggest that the influence of this transcription factor extends beyond the B cell lineage.
Contact hypersensitivity is a form of delayed-type hypersensitivity, a classic T cell–mediated, clinically important phenomenon. Unexpectedly, a new study indicates that natural killer cells may mediate contact hypersensitivity and demonstrate adaptive, memory-like activity.
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.
