Imiquimod (AldaraTM), a Toll-like receptor 7 agonist (TLR7), is known for its unique properties of being an immune response modifier and stimulator. Upon topical application, this TLR7 agonist triggers a cell-mediated immune response predominantly expressed by dendritic cells and monocytes. Local skin irritation at the application site involving erythema, pain, crusting and erosions is common and well documented. On the contrary, the specific histopathologic features associated with these treatment site reactions is not. Herein reported is a case where historical omission of imiquimod use for actinic keratosis complicated the histologic interpretation. We highlight a lupus erythematosus-like microscopic pattern and explore histopathologic features that could help in avoiding a diagnostic pitfall, as well as the relationship between TLR activation, cell-mediated immunity and skin histology.
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http://dx.doi.org/10.1111/j.1600-0560.2010.01592.x | DOI Listing |
Clin Case Rep
January 2025
Rheumatic Diseases Research Center, Ghaem Hospital, Taghi Abad Mashhad University of Medical Sciences Mashhad Iran.
When systematic lupus erythematosus-like lab results (e.g., positive anti-double-stranded DNA antibody, low complement component 3) are inconsistent with physical findings, such as the absence of arthritis or nephritis, clinicians should consider diagnoses such as Wilson's disease, especially in the presence of abnormal liver function and elevated international normalized ratio (INR).
View Article and Find Full Text PDFJ Dermatol
November 2024
Department of Dermatology, Mie University Hospital, Tsu, Japan.
iScience
November 2024
Department of Immunology, School of Basic Medical Sciences, Fudan University, Shanghai, China.
Curr Opin Allergy Clin Immunol
December 2024
Paediatric Stem Cell Transplant Unit, Great North Children's Hospital, Newcastle upon Tyne, United Kingdom.
Purpose Of Review: C1q deficiency is a rare inborn error of immunity characterized by susceptibility to severe infections and profound immune dysregulation, with a systemic lupus erythematosus-like phenotype. The management of patients with C1q deficiency is challenged by the rarity of this condition and the wide clinical variability. This review aims to emphasize the importance of a thorough immunological and clinical characterization to help guide a personalized and comprehensive approach to patients.
View Article and Find Full Text PDFACR Open Rheumatol
December 2024
Medical University of South Carolina and Ralph H. Johnson VA Health Care System, Charleston.
Objective: Systemic lupus erythematosus (SLE) affects nine women to every man worldwide, and these patients are at greater risk for cardiovascular disease (CVD) morbidity and mortality. Clinical studies have demonstrated that patients with SLE are more likely to develop CVD, including cardiac and vascular dysfunction. Although many preclinical models of SLE are available, including treatment with Toll-like receptor (TLR) 7/8 agonists, a consistent preclinical model of SLE-like CVD with systemic, cardiac, renal, and cerebral endothelial activation and cardiac dysfunction has yet to be described.
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