Publications by authors named "E R Wilfong"

Article Synopsis
  • Interstitial lung disease (ILD) frequently occurs in adults with idiopathic inflammatory myopathies, particularly those with antisynthetase syndrome and anti-MDA5 antibodies, manifesting in various severities from mild to rapidly worsening symptoms.
  • Common symptoms include lung issues along with myositis, skin lesions, arthritis, and Raynaud’s phenomenon, but 16-65% may have lung problems as the only indication.
  • Treatment typically involves immunosuppression, combining therapies for aggressive cases, and possibly lung transplantation for severe cases, although short-term mortality is notably high in rapidly progressive disease associated with anti-MDA5 antibodies.
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An increased risk of cardiometabolic disease accompanies persistent systemic inflammation. Yet, the innate and adaptive immune system features in persons who develop these conditions remain poorly defined. Doublets, or cell-cell complexes, are routinely eliminated from flow cytometric and other immune phenotyping analyses, which limits our understanding of their relationship to disease states.

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Although profibrotic cytokines, such as IL-17A and TGF-β1, have been implicated in the pathogenesis of interstitial lung disease (ILD), the interactions between gut dysbiosis, gonadotrophic hormones and molecular mediators of profibrotic cytokine expression, such as the phosphorylation of STAT3, have not been defined. Here, through chromatin immunoprecipitation sequencing (ChIP-seq) analysis of primary human CD4+ T cells, we show that regions within the STAT3 locus are significantly enriched for binding by the transcription factor estrogen receptor alpha (ERa). Using the murine model of bleomycin-induced pulmonary fibrosis, we found significantly increased regulatory T cells compared to Th17 cells in the female lung.

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Persons with HIV (PWH) on long-term antiretroviral therapy (ART) have a higher incidence and prevalence of cardiometabolic diseases attributed, in part, to persistent inflammation despite viral suppression. In addition to traditional risk factors, immune responses to co-infections such as cytomegalovirus (CMV) may play an unappreciated role in cardiometabolic comorbidities and offer new potential therapeutic targets in a subgroup of individuals. We assessed the relationship of CX3CR1, GPR56, and CD57 T cells (termed CGC) with comorbid conditions in a cohort of 134 PWH co-infected with CMV on long-term ART.

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