Volume 14 Issue 3, March 2013

By increasing the range of epitopes presented to lymphocytes, determinant spreading allows a more diverse response to ensue. Now the cellular culprits responsible for determinant spreading in the central nervous system have been identified: they are specialized dendritic cells that recruit CD8⁺ T cells to an autoimmune 'crime'.

The differentiation of monocytes is altered in cancer, which results in the unexpected conversion of a large proportion of monocytic myeloid-derived suppressor cells into polymorphonuclear myeloid-derived suppressor cells.

The fate of T cells differentiating into the CD4 or CD8 lineage is typically fixed when cells leave the thymus. However, CD4⁺ helper T cells can be reprogrammed to develop into CD4⁺CD8α⁺ cytotoxic T lymphocytes in the gut.

The Nr4a family of transcription factors transactivate expression of the transcription factor Foxp3 and are essential for the generation of regulatory T cells. Mice deficient in all three members of the Nr4a family develop massive multiorgan inflammation.

Gabrilovich and colleagues show that monocytic myeloid-derived suppressor cells (MDSCs) differentiate into polymorphonuclear MDSCs in individuals with tumors, demonstrating a demonstrating a distinct regulation of myeloid cell development in cancer.

Innate lymphoid cells are cytokine-producing cells that contribute to tissue homeostasis. Spits and colleagues identify a human innate cell population that expresses T-bet and IFN-γ and is prevalent in Crohn's disease.

Sekiya and colleagues demonstrate that the Nr4a nuclear receptors, which are encoded by immediate-early genes upregulated by TCR stimulation in thymocytes, have an essential role in regulatory T cell development.

Villadangos and colleagues show that lung resident memory CD8⁺ T cells selectively maintain expression of IFITM3, a protein that confers broad resistance to viral infection.

Unlike vaccination, infection by a live pathogen often impairs dendritic cell function. Iwasaki and colleagues show that during infection with influenza virus, signaling via the IL-1 receptor is both required and sufficient for the priming of CD8⁺ T cells.

Autoreactive CD8⁺ T cells are prevalent in multiple sclerosis. Goverman and colleagues identify tumor necrosis factor–inducible nitric oxide synthase (TNF-iNOS)-producing dendritic cells that cross-present myelin antigen to activate naive CD8⁺ T cells in the central nervous system.

Vignali and colleagues show that a full complement of ITAMs is required in the TCR-CD3 complex for TCR-driven T cell proliferation, whereas a low number of functional ITAMs is sufficient for cytokine secretion.

CD4⁺ and CD8⁺ T cells are considered distinct functional lymphocyte subsets. Cheroutre and Mucida and their colleagues show that mature gut-associated CD4⁺ T cells lose ThPOK expression and reactivate CD8 cytolytic effector programs.

CD4⁺ and CD8⁺ T cells are considered distinct functional lymphocyte subsets. Cheroutre and Mucida and their colleagues show that mature gut-associated CD4⁺ T cells lose ThPOK expression and reactivate CD8 cytolytic effector programs.

Tarlinton and colleagues show that the antiapoptotic protein Mcl1 is essential for plasma cell survival and is induced by BCMA signaling in bone marrow, but not spleen, plasma cells.

Plasma cells are antibody 'factories', which places considerable metabolic stress on these cells. Cenci and colleagues show that long-lived plasma cells and sustained antibody production require autophagy activation.