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Caveolin-1 has a critical role in orchestrating the membrane organization of B cells. In its absence, signaling via the B cell antigen receptor and B cell tolerance are impaired, which results in autoimmunity.
Lambrecht and Hammad discuss how microbial diversity or dysbiosis influences epithelial barrier tissues and the impact of such interactions on the development of allergic disease.
Kaplan reviews the development of skin-resident Langerhans cells and their unique functional roles that distinguish these cells from other skin antigen-presenting cells.
Poor glycolysis and increased fatty-acid synthesis feed the locomotion machinery in T cells from people with rheumatoid arthritis and allow these cells to enter the synovium and propagate joint inflammation and destruction.
The ability to expand and contract populations of myeloid and lymphoid cells during emergency hematopoiesis helps shape the immune response. The expression of intracellular and soluble forms of osteopontin regulates apoptosis thresholds differently in myeloid cells and lymphoid cells to counter infection.
The histone lysine methyltransferase MLL4 primes the locus encoding the transcription factor Foxp3 for transcriptional activation in thymus-derived and inducible regulatory T cells.
The cytokine TGF-β allows tumors to evade the immune system by converting conventional natural killer cells into type 1 innate lymphoid cells devoid of cytotoxic function.
Long non-coding RNAs (lncRNAs) are being increasingly appreciated as important regulators of gene expression. Chang and colleagues review the roles identified for lncRNAs in the immune system and discuss models for how lncRNAs mediate their effects.
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.
Kroemer and colleagues discuss the mechanisms through which nutrition modulates metabolic, microbial and neuroendocrine circuitries that affect cancer development and the response to treatment.
Beyaert, Karin and colleagues discuss the key molecular mechanisms that contribute to the self-limiting nature of inflammatory signaling, with emphasis on the negative regulation of the NF-κB pathway and the NLRP3 inflammasome.
Magarian Blander and colleagues review the effects of the microbiome on innate and adaptive immunological players and how microbiota-derived bioactive molecules affect inflammation and the host response to infection, vaccination and cancer.
Kastner and colleagues review monogenic autoinflammatory diseases and their molecular mechanisms and explore the overlap among autoinflammation, autoimmunity and immunodeficiency.
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.
Autoimmunity can arise when tolerance mechanisms break down. Theofilopoulos and colleagues review how loss of peripheral tolerance, often driven by innate nucleic-acid sensors, leads to the activation of autoreactive lymphocytes that underlie many autoimmune diseases.
