Antimicrobial responses articles from across Nature Portfolio

An amino acid metabolic enzyme transforms bacterial lipoproteins into disulfide-linked lipid structures that activate the non-canonical inflammasome, redefining cytosolic innate immune sensing as a process shaped by host metabolic remodeling.

Cao et al. report that whole β-glucan particles (WGP) enhance BCG-conditioned macrophage antigen handling and presentation. WGP plus BCG strengthens CD4⁺ memory-associated responses and improves bacterial control while reducing lung inflammation

Here, the authors show that bacteria release immunosuppressive lipopeptides that suppress eczema and may serve as a potential therapy. This activity is independent of toll-like receptor signalling but involves gasdermin D-induced release of IL-33.

This Primer by Strle and colleagues summarizes the epidemiology, pathophysiology, diagnosis and treatment of Lyme borreliosis.

The fine deciphering of host immune responses of the different cattle subspecies towards vector-borne viruses highlighted clear distinctions. These different immune responses are likely to correlate with a differential control of the pathogen.

An amino acid metabolic enzyme transforms bacterial lipoproteins into disulfide-linked lipid structures that activate the non-canonical inflammasome, redefining cytosolic innate immune sensing as a process shaped by host metabolic remodeling.

A mycovirus drives the fitness of the lung-infecting fungus Aspergillus fumigatus under stress, helping it to survive within immune cells, and thus shaping its pathogenesis.

Giardia intestinalis is a protozoan parasite that can cause severe enteric disease. The immune response to this organism provides unexpected benefits to limit gut inflammation.

A preprint by McCaffrey and Delmastro et al. delineates distinct immunometabolic zones of tuberculosis granulomas and reports that hypoxia is a key driver of immune subversion.

White et al. show that microbiota-specific T cells are licensed by gut inflammation to infiltrate the central nervous system, where cross-reactivity with self-antigens leads to neuropathology.

A preprint by Cheng et al. identifies the proton-activated chloride channel PAC as a negative regulator of phagosomal acidification in macrophages.