Objective: Cutaneous anergy testing evaluates delayed type hypersensitivity responses and is, in essence, an in-vivo measure of cell-mediated immune function at an epithelial surface. This study assessed the relationship of anergy test results with cervical infection by human papillomavirus (HPV) and cervical neoplasia in HIV-seropositive and seronegative women.
Methods: HIV-seropositive (n = 1029) and HIV-seronegative (n = 272) women enrolled in a long-term cohort study were followed semi-annually with HPV-DNA testing and cytology. Anergy was defined as unresponsiveness to Candida albicans, tetanus toxoid, and mumps antigen.
Results: Anergy was associated with the prevalent detection of squamous intraepithelial lesions [SIL; adjusted odds ratio 1.70; 95% confidence interval (CI) 1.16-2.48] in multivariable logistic regression models, and with the incident detection of oncogenic HPV (adjusted hazard ratio 1.24; 95% CI 0.99-1.56) in multivariable Cox regression models. These models adjusted for HIV infection, combined CD4 T-cell and HIV-RNA strata (13 separate strata to control optimally for their interactive effects), as well as other variables.
Conclusion: Cutaneous anergy testing may measure aspects of local cellular immune function in epithelial tissues that are important for the control of HPV and development of SIL, and that in HIV-seropositive women are not fully accounted for by circulating CD4 T-cell counts and HIV-RNA levels.
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http://dx.doi.org/10.1097/QAD.0b013e3282c3a945 | DOI Listing |
Clin Immunol
October 2023
Department of Pharmacology & Molecular Therapeutics, Uniformed Services University of the Health Sciences, Bethesda, MD, USA. Electronic address:
Pathogens
June 2023
Centro de Agravos Tropicais Emergentes e Negligenciados, Universidade Federal do Piauí, Teresina 64000-450, PI, Brazil.
Infection with and may lead to diffuse cutaneous leishmaniasis. The cure is exceptional, especially for the strange case of this lady. Case report: The patient acquired the disease in childhood and remained with lesions for over 30 years, albeit several treatments.
View Article and Find Full Text PDFVet Q
December 2023
Center of Excellence for Companion Animal Cancer, Department of Veterinary Pathology, Faculty of Veterinary Science, Chulalongkorn University, Bangkok, Thailand.
Immune escape is the hallmark of carcinogenesis. This widely known mechanism is the overexpression of immune checkpoint ligands, such as programmed cell death protein 1 and programmed death-ligand 1 (PD-1/PD-L1), leading to T cell anergy. Therefore, cancer immunotherapy with specific binding to these receptors has been developed to treat human cancers.
View Article and Find Full Text PDFNature
July 2023
Department of Immunobiology, Yale University School of Medicine, New Haven, CT, USA.
The peripheral T cell repertoire of healthy individuals contains self-reactive T cells. Checkpoint receptors such as PD-1 are thought to enable the induction of peripheral tolerance by deletion or anergy of self-reactive CD8 T cells. However, this model is challenged by the high frequency of immune-related adverse events in patients with cancer who have been treated with checkpoint inhibitors.
View Article and Find Full Text PDFFront Immunol
March 2023
Garvan Institute of Medical Research, Sydney, NSW, Australia.
Introduction: Germline CARD11 gain-of-function (GOF) mutations cause B cell Expansion with NF-κB and T cell Anergy (BENTA) disease, whilst somatic GOF CARD11 mutations recur in diffuse large B cell lymphoma (DLBCL) and in up to 30% of the peripheral T cell lymphomas (PTCL) adult T cell leukemia/lymphoma (ATL), cutaneous T cell lymphoma (CTCL) and Sezary Syndrome. Despite their frequent acquisition by PTCL, the T cell-intrinsic effects of CARD11 GOF mutations are poorly understood.
Methods: Here, we studied B and T lymphocytes in mice with a germline Nethyl-N-nitrosourea (ENU)-induced Card11 mutation identical to a mutation identified in DLBCL and modifying a conserved region of the CARD11 coiled-coil domain recurrently mutated in DLBCL and PTCL.
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