Background: Oral warts, caused by human papillomavirus (HPV), and oral hairy leukoplakia (OHL) caused by Epstein-Barr virus (EBV), are common oral manifestations in HIV-infected persons. Although both conditions occur most often with reduced blood CD4+ T-cell numbers, oral warts and OHL rarely occur simultaneously, suggesting that dysfunctions in other secondary local immune parameters are also involved. The present study evaluated tissue-associated proinflammatory and T-helper cytokine and chemokine mRNA expression and the presence of T cells in each lesion.
Methods: Biopsies were taken from lesion-positive and adjacent lesion-negative sites of HIV+ persons with oral warts or OHL and lesion-negative sites from HIV+ persons who were oral HPV or EBV DNA-positive (matched controls). Cytokine/chemokine mRNA expression was quantified by real-time polymerase chain reaction. CD3, CD4, and CD8 cells were identified by immunohistochemistry.
Results: No differences were detected in tissue-associated cytokine/chemokine mRNA expression in warts or OHL when compared to lesion-negative sites. Immunohistochemical analysis of T cells showed CD8+ cells exclusively, but few cells were present in either lesion. No differences were detected between lesion-positive and -negative control sites of each pathologic condition.
Conclusion: Little evidence was found for local immune reactivity to either oral warts and OHL, suggesting that CD4+ T cells are a primary host defense against both oral warts and OHL, but with nonimmune factors potentially responsible for the divergent prevalence of each.
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http://dx.doi.org/10.1111/j.1399-302X.2005.00198.x | DOI Listing |
Asian Pac J Cancer Prev
November 2024
Department of Restorative and Prosthetic Dental Sciences, College of Dentistry, Dar Al Uloom University, Riyadh, Saudi Arabia.
Front Immunol
November 2024
Université Paris Cité, Institut de Recherche Saint-Louis, INSERM U1160, Paris, France.
Background: WHIM (Warts, Hypogammaglobulinemia, Infections, and Myelokathexis) syndrome is an ultra-rare, combined primary immunodeficiency and chronic neutropenic disorder characterized by a range of clinical presentations, including peripheral neutropenia, lymphopenia, and recurrent infections. WHIM syndrome is most often caused by gain-of-function mutations in the gene encoding C-X-C chemokine receptor 4 (CXCR4). As such, inhibition of CXCR4 with XOLREMDI (mavorixafor), an orally bioavailable CXCR4 antagonist, demonstrated clinically meaningful increases in absolute neutrophil and lymphocyte counts and concomitant reduction in infections in patients with WHIM syndrome, resulting in its recent U.
View Article and Find Full Text PDFJ Cancer Educ
December 2024
Laboratory of Research in Health Sciences and Technologies, Higher Institute of Health Sciences, Hassan First University of Settat, BP 555, Settat, Morocco.
Infect Agent Cancer
October 2024
Department of Obstetrics and Gynecology, Catholic University of Health and Allied Sciences, Bugando, P. O. Box 1464, Mwanza, Tanzania.
J Dermatol
January 2025
Department of Social and Environmental Medicine, Kanazawa Medical University, Kanazawa, Ishikawa, Japan.
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