Screening for transcriptomic associations with Swine Inflammation and Necrosis Syndrome.

Background: The recently identified swine inflammation and necrosis syndrome (SINS) affects tail, ears, teats, coronary bands, claws and heels of affected individuals. The primarily endogenous syndrome is based on vasculitis, thrombosis, and intimal proliferation, involving defence cells, interleukins, chemokines, and acute phase proteins and accompanied by alterations in clinical chemistry, metabolome, and liver transcriptome. The complexity of metabolic alterations and the influence of the boar led to hypothesize a polygenic architecture of SINS.

Lipidic folding pathway of α-Synuclein via a toxic oligomer.

Aggregation intermediates play a pivotal role in the assembly of amyloid fibrils, which are central to the pathogenesis of neurodegenerative diseases. The structures of filamentous intermediates and mature fibrils are now efficiently determined by single-particle cryo-electron microscopy. By contrast, smaller pre-fibrillar α-Synuclein (αS) oligomers, crucial for initiating amyloidogenesis, remain largely uncharacterized.

Enhancing NK cell-mediated tumor killing of B7-H6 cells with bispecific antibodies targeting allosteric sites of NKp30.

In this work, we report the discovery and engineering of allosteric variable domains of the heavy chain (VHHs) derived from camelid immunization targeting NKp30, an activating receptor on natural killer (NK) cells. The aim was to enhance NK cell-mediated killing capacities by identifying VHHs that do not compete with the natural ligand of NKp30:B7-H6, thereby maximizing the recognition of B7-H6 tumor cells. By relying on the DuoBody technology, bispecific therapeutic antibodies were engineered, creating a panel of bispecific antibodies against NKp30xEGFR (cetuximab moiety) or NKp30xHER2 (trastuzumab moiety), called natural killer cell engagers (NKCEs).

Microcephaly protein ANKLE2 promotes Zika virus replication.

Orthoflaviviruses are positive-sense single-stranded RNA viruses that hijack host proteins to promote their own replication. Zika virus (ZIKV) is infamous among orthoflaviviruses for its association with severe congenital birth defects, notably microcephaly. We previously mapped ZIKV-host protein interactions and identified the interaction between ZIKV non-structural protein 4A (NS4A) and host microcephaly protein ankyrin repeat and LEM domain-containing 2 (ANKLE2).