Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
The infiltration of solid tumors by CD8+ T cells is a favorable prognostic marker. Large-scale transcriptome analysis of tumor-infiltrating T cells from mucosal tumors shows that CD8+ T cells with a CD103+ tissue-resident memory T cell phenotype might be the most desirable.
Lineage bias among early hematopoietic progenitor cells is specified by transcription-factor programming, and lineage switching reduces the quantity of cells produced.
Chemokines are important components of the hematopoietic niche. The atypical chemokine receptor 1 (ACKR1), expressed on erythrocyte precursors, regulates myeloid differentiation.
Thymocytes must undergo positive selection to survive and differentiate. This process is regulated by the TCR-sensitive protein CHMPS by preventing Bcl2 oxidation and degradation.
A study of polymorphisms in the sensor IFIH1 exposes the evolutionary trade-off between a robust antiviral type I interferon response and the risk of interferon-mediated inflammation.
The Hippo signaling pathway regulates cellular proliferation and survival during tissue growth and cancer. In CD4+ T cells, members of the Hippo family modulate autoimmune inflammation by altering interactions between the transcription factors Foxp3 and RORγt; this reveals an unexpected non-canonical role for Hippo in adaptive immunity.
M cells sample gut lumenal antigens and microbes to induce gut immune responses. A novel population of stromal cell—the M cell inducers—are essential for sustaining M cell differentiation and bacteria-specific production of immunoglobulin A to maintain the gut–immune system symbiosis.
The transcription factor STAT5 acts as an oncoprotein in B cell acute lymphoblastic leukemia, competing with the transcription factors NF-κB and Ikaros for binding to DNA.
Monocytes recruited to the peritoneum under conditions of a type 2 inflammatory reaction can convert into resident-type macrophages under the control of vitamin A.
RNA-binding proteins (RBPs) take control of binary cell-fate 'decisions' and cellular identity in lymphoid organs, as the RBP ZFP36L1 is shown to negatively regulate the stability of the transcription factors KLF2 and IRF8 to control the maintenance, survival and localization of marginal zone B cells.
IRE1α is a stress sensor that is activated by a high-fat diet. In adipose-tissue macrophages, it serves as a major switch toward pro-inflammatory M1 polarization and thereby contributes to obesity and associated diseases.
The immune system employs a multitude of molecules, cells and organs that act together throughout the entire body to guard human health. Much like in a social network, immune cells can exert full functionality only through effective collaboration and communication.
The transcription factor IRF4 acts as a 'rheostat' for TCR signaling. Discrete levels of IRF4 can activate distinct transcriptional programs in T cells due to binding sites of variable affinity in groups of target genes.
The short-chain fatty acids (SCFAs) acetate and butyrate, which are released from specialized diets by gut microbes, protect non-obese diabetic (NOD) mice against insulitis and slow the progression of diabetes.
Antibodies to neutralizing epitopes on hemagglutinin exhibit reproducible dynamic immunodominance patterns over time. Early responses target largely the Cb site, followed by Sb dominance and a concomitant rise in the diversity of neutralizing-antibody specificities.
THEMIS, the enigmatic regulator of T cell selection in the thymus, controls selection by oxidizing and suppressing the activity of the tyrosine phosphatase SHP-1.
Throughout ontogeny, the γδ TCR repertoire in human blood becomes less diverse and more focused, yet is private in nature, and specific adult γδ T cell subsets undergo substantial clonal expansion after challenge with cytomegalovirus.