Pink verrucous plaque in a man with systemic mastocytosis

Porokeratosis ptychotropica is a rare and commonly misdiagnosed subtype of porokeratosis involving the body folds. We present a 53-year-old man with systemic mastocytosis who presented with a pruritic, verrucous plaque in the gluteal fold that showed multiple cornoid lamellae on histopathologic evaluation, diagnostic of porokeratosis ptychotropica. Various treatments have been reported, including topical corticosteroids, retinoids, vitamin D analogs, calcineurin inhibitors, imiquimod, phototherapy, cryotherapy, or ablative laser therapy, but recurrences are common

Eosinophilic fasciitis presenting as a unilateral, solitary plaque

Eosinophilic fasciitis is a rare connective tissue disorder characterized by inflammation of the fascia that leads to painful, indurated skin. Because of its variable clinical presentation and overlap with conditions, such as morphea, the diagnosis of eosinophilic fasciitis can be challenging and relies on clinical presentation, histopathologic and laboratory analysis, and response to therapy. Herein, we present an unusual, solitary, isolated plaque with pathologic features and response to therapy most consistent with eosinophilic fasciitis

Delayed maturation of an IL-12–producing dendritic cell subset explains the early Th2 bias in neonatal immunity

Primary neonatal T cell responses comprise both T helper (Th) cell subsets, but Th1 cells express high levels of interleukin 13 receptor α1 (IL-13Rα1), which heterodimerizes with IL-4Rα. During secondary antigen challenge, Th2-produced IL-4 triggers the apoptosis of Th1 cells via IL-4Rα/IL-13Rα1, thus explaining the Th2 bias in neonates. We show that neonates acquire the ability to overcome the Th2 bias and generate Th1 responses starting 6 d after birth. This transition was caused by the developmental maturation of CD8α+CD4− dendritic cells (DCs), which were minimal in number during the first few days of birth and produced low levels of IL-12. This lack of IL-12 sustained the expression of IL-13Rα1 on Th1 cells. By day 6 after birth, however, a significant number of CD8α+CD4− DCs accumulated in the spleen and produced IL-12, which triggered the down-regulation of IL-13Rα1 expression on Th1 cells, thus protecting them against IL-4–driven apoptosis

Innocuous IFNγ induced by adjuvant-free antigen restores normoglycemia in NOD mice through inhibition of IL-17 production

The role of Th17 cells in type I diabetes (TID) remains largely unknown. Glutamic acid decarboxylase (GAD) sequence 206–220 (designated GAD2) represents a late-stage epitope, but GAD2-specific T cell receptor transgenic T cells producing interferon γ (IFNγ) protect against passive TID. Because IFNγ is known to inhibit Th17 cells, effective presentation of GAD2 peptide under noninflammatory conditions may protect against TID at advanced disease stages. To test this premise, GAD2 was genetically incorporated into an immunoglobulin (Ig) molecule to magnify tolerance, and the resulting Ig-GAD2 was tested against TID at different stages of the disease. The findings indicated that Ig-GAD2 could not prevent TID at the preinsulitis phase, but delayed TID at the insulitis stage. More importantly, Ig-GAD2 sustained both clearance of pancreatic cell infiltration and β-cell division and restored normoglycemia when given to hyperglycemic mice at the prediabetic stage. This was dependent on the induction of splenic IFNγ that inhibited interleukin (IL)-17 production. In fact, neutralization of IFNγ led to a significant increase in the frequency of Th17 cells, and the treatment became nonprotective. Thus, IFNγ induced by an adjuvant free antigen, contrary to its usual inflammatory function, restores normoglycemia, most likely by localized bystander suppression of pathogenic IL-17–producing cells

Coordinate regulation of GATA3 and CD4+ T-helper 2 (TH2) cytokine gene expression by the RNA-binding protein HuR [abstract]

Asthma and other allergic inflammation diseases are major contributors to hospitalizations and deaths worldwide. These diseases are the result of over reactive immune responses initiating pro inflammatory mediators. These CD4+ T helper type 2 (Th2) mediated diseases are driven by the transcription factor GATA3 as well as the cytokines IL-4 and IL-13. HuR, an RNA binding protein (RBP), has been shown to posttranscriptionally regulate many early response genes, including these critical allergy mediators

Second degree burn to mustard powder

Mustard seeds and powder are commonly used inhomeopathic and traditional medicines, in whichthey are believed to have both anti-microbial andanti-inflammatory properties. They are thereforeutilized in the treatment of conditions ranging fromarthritis to respiratory congestion. Herein, we presenta patient with a second degree burn who usedmustard powder in the form of a mustard plasterto treat chest congestion. She experienced seconddegree burn wounds to the lower neck and chest, andrecovery with complete re-epithelialization followingtopical silver sulfadiazine, liberal emollient therapy,and triamcinolone ointment. This case highlightsthe potential danger of inappropriate use of topicalhomeopathic remedies such as mustard powder anddetails a successful treatment regimen

Second degree burn to mustard powder

Mustard seeds and powder are commonly used inhomeopathic and traditional medicines, in whichthey are believed to have both anti-microbial andanti-inflammatory properties. They are thereforeutilized in the treatment of conditions ranging fromarthritis to respiratory congestion. Herein, we presenta patient with a second degree burn who usedmustard powder in the form of a mustard plasterto treat chest congestion. She experienced seconddegree burn wounds to the lower neck and chest, andrecovery with complete re-epithelialization followingtopical silver sulfadiazine, liberal emollient therapy,and triamcinolone ointment. This case highlightsthe potential danger of inappropriate use of topicalhomeopathic remedies such as mustard powder anddetails a successful treatment regimen

Livedo racemosa secondary to hyaluronic acid injection

Iatrogenic vascular occlusion secondary to filler injection, such as with hyaluronic acid, is a known but rare, entity. It typically occurs in the setting of facial cosmetic procedures but has also been described in the setting of osteoarthritis. We present a patient with ankle osteoarthritis who developed an asymmetric, reticular, livedoid eruption after intraarticular injection with hyaluronic acid. She was diagnosed with livedo racemosa secondary to vascular occlusion and placed on low molecular weight heparin. Later, a transition to low-dose daily aspirin maintained the improvement