Browse our latest Immunology and Inflammation articles

A new mouse model of sepsis can reproduce the long-term muscle weakness seen in patients who survive this life-threatening illness.

Intravital imaging with HIV-1 viral-like particle in mouse model reveals a mechanism for HIV-1 uptake by subcapsular sinus macrophages that facilitates HIV-1 spreading tofollicular dendritic and B cells.

Sepsis-induced long-term muscle weakness was reproduced using a refined murine model, which was accompanied by mitochondrial dysfunction in the absence of sustained atrophy, suggesting the promise of mitochondria-targeted post-sepsis therapies.

Neutrophils are essential for itch in a mouse model of atopic dermatitis, and promote the transition from acute to chronic itch via induction of CXCL10/CXCR3 signaling.

Feedback from the intestine during infection can modulate the behavior, learning, and microbial perception of the host.

Neutrophils are the first immune cells that enter the skin and cause itch in atopic dermatitis.

An ancient integration of an endogenous retroelement in the gene encoding PD-L1 is exapted to generate a soluble form that antagonises the suppressive function of the membrane-bound form.

Activated Drosophila macrophages undergo transient metabolic remodeling towards Hypoxia inducible factor 1 α-driven aerobic glycolysis, a program that induces systemic metabolic changes and is crucial for resistance to infection.

The association of atypical memory B-cells and autoimmune antibodies (anti-phosphatidylserine) with hemoglobin levels in malaria patients uncovers a novel mechanism for the human malaria-induced anemia previously identified in mice.

Targeting ErbB receptor tyrosine kinases modifies neutrophil survival and inflammation across multiple species, and reveals a new use for ErbB therapeutics in resolving inflammatory disease.