Bacterial immune evasion articles from across Nature Portfolio

Bacterial type IV pili are filamentous cell surface structures and candidate targets for vaccine development. Here, authors determine how antibodies interact with pili at the structural level providing insight into immune escape mechanisms and potential countermeasures.

This Review provides an updated assessment of the expanding family of T cell-activating bacterial superantigens, emphasizing potential roles of these toxins in various disease states as well as their contribution to the evolution of the bacterial pathogens Staphylococcus aureus and Streptococcus pyogenes.

Intracellular bacteria use deubiquitinase effectors to avoid being targeted for autophagic clearance. The authors show that the Chlamydia-like bacterium Simkania negevensis encodes an unusually broad range of these enzymes, including members that specifically target linear and K6-linked ubiquitin chains.

Here, the authors used cryo-EM to explore secretory Immunoglobulin A interactions with bacterial and host receptors, uncovering unexpected binding stoichiometry and unappreciated functional consequences relevant to understanding host-pathogen interactions.

Legionella pneumophilia is known to secrete more than 300 effectors via a type IV secretion system. Here, Schator et al. characterise how the chromatin modifying effectors RomA and LphD work synergistically to hijack host responses and facilitate bacterial replication.

This study uncovers how Yersinia pestis is protected from engulfment by macrophages by the capsule-like antigen F1.

This study shows that Salmonella enterica subsp. enterica serovar Typhimurium virulence and survival are modulated by changes in host cell metabolism during infection.

A recent study found that Mycobacterium tuberculosis infection in mice reprogrammes haematopoietic stem cells, limiting myelopoiesis and impairing trained immunity.

Host cells assemble linear ubiquitin chains to activate immune signalling during bacterial infection. A new study reveals that Legionella pneumophila — the causative agent of Legionnaires’ disease — produces an enzyme that specifically disassembles these linear ubiquitin modifications to restrict immune responses.

This study found that a lipase secreted by the opportunistic pathogen Staphylococcus aureus promotes immune evasion.

Molecular players involved in systemic and acute infections are relatively easy to pinpoint, whereas bacterial resilience during chronic infections remains less well understood. Pseudomonas aeruginosa encodes a quorum-regulated virulence factor, TesG, that promotes chronic lung infection by suppressing host inflammatory responses.