Browse our latest Immunology and Inflammation articles

A short treatment of the NOD mouse model of type-1 diabetes with I-BET151, a small molecule bromodomain blocker, provides long-term protection from disease by inducing macrophages to adapt an anti-inflammatory tenor whilst promoting islet β cell regeneration.

Genetic susceptibility to an infectious disease is linked to competition for binding a molecule on the bacterial surface by two host proteins with opposing roles in host immunity.

MHC class II-mediated self-antigen presentation by lymph node stromal cells controls regulatory T cell homeostasis, thus safeguarding immune tolerance.

Contrary to the current perception, insect eggs are very capable of defending themselves against pathogens.

The adaptor proteins FADD and TRADD play an important role in the Sharpin-dependent anti-apoptosis signaling pathway in keratinocytes and regulate skin homeostasis.

The co-stimulatory molecule CD28 is required after T cell priming for helper T cell polarization in response to an infection.

Autophagy is required for CD8⁺ T cell memory formation; in aged individuals autophagy levels are diminished, and increasing autophagy enhances their CD8⁺ T cell responses.

The transcription factor NFIL3 is essential for the development of a committed bone marrow precursor that gives rise to all known innate lymphoid cell lineages in mice.

Activation of lung macrophage nitric oxide synthase-3 improves both bacterial clearance and outcome in primary and secondary pneumonia models.