Immunization with modified vaccinia virus Ankara prevents eczema vaccinatum in a murine model of atopic dermatitis.

Immunization with modified vaccinia virus Ankara (MVA) protects mice with allergic skin inflammation from developing eczema vaccinatum (EV), suggesting that immunization with MVA would be effective in preventing EV in patients with atopic dermatitis.

The prostaglandin D₂ receptor CRTH2 is important for allergic skin inflammation after epicutaneous antigen challenge.

Background: Cutaneous prostaglandin (PG) D₂ levels increase after scratching. Chemoattractant receptor-homologous molecule expressed on receptor on T(H)2 cells (CRTH2) mediates chemotaxis to PGD₂ and is expressed on T(H)2 cells and eosinophils, which infiltrate skin lesions in patients with atopic dermatitis.

Objective: We sought to examine the role of CRTH2 in a murine model of atopic dermatitis.

Misexpression of Pou3f1 results in peripheral nerve hypomyelination and axonal loss.

Pou3f1/SCIP/Oct-6 is a POU-domain transcription factor that is an important regulator of peripheral nerve myelination by Schwann cells. Pou3f1-deficient mice experience a developmental delay in myelination indicating that transient induction of Pou3f1 is required for normal development of peripheral myelin. The mechanism by which Pou3f1 regulates myelination is unclear, because it can both increase expression of Egr2, a transcription factor that promotes the myelination program, and also repress the promoters of specific myelin genes such as myelin protein zero (MPZ) and myelin basic protein (MBP).

Nab proteins are essential for peripheral nervous system myelination.

Mutations that disrupt Egr2 transcriptional activity cause severe demyelinating peripheral neuropathies. Here we provide evidence that Nab1 and Nab2 proteins are critical transcriptional modulators of Egr2 in myelinating Schwann cells. Like Egr2, these proteins are essential for Schwann cell differentiation into the myelinating state.

Analysis of congenital hypomyelinating Egr2Lo/Lo nerves identifies Sox2 as an inhibitor of Schwann cell differentiation and myelination.

Egr2 is a transcription factor required for peripheral nerve myelination in rodents, and mutations in Egr2 are associated with congenital hypomyelinating neuropathy (CHN) in humans. To further study its role in myelination, we generated mice harboring a hypomorphic Egr2 allele (Egr2Lo) that survive for up to 3 weeks postnatally, a period of active myelination in rodents. These Egr2Lo/Lo mice provided the opportunity to study the molecular effects of Egr2 deficiency on Schwann cell biology, an analysis that was not possible previously, because of the perinatal lethality of Egr2-null mice.