DEFECTIVE ACTIVATION OF DENDRITIC CELLS IN A CASE OF LOCALLY INVASIVE ASPERGILLOSIS
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Tipo de produção
conferenceObject
Data de publicação
2012
Título da Revista
ISSN da Revista
Título do Volume
Editora
SPRINGER/PLENUM PUBLISHERS
Autores
DIAS, A. Santos
ALVES, C.
Citação
JOURNAL OF CLINICAL IMMUNOLOGY, v.32, suppl.1, p.88-88, 2012
Resumo
Primary immunodeficiencies are rare and usually first manifest during childhood. Invasive aspergillosis is the leading cause of mortality in phagocyte defects, reflecting the key role of these cells in the host defense against opportunistic fungi. Patients with AD STAT-3 de ficiency are prone to colonization of lung cavities (pneumatoceles) by Aspergillus species leading to local invasion and rarely disseminated infection. Other phagocytic and T-cell disorders are uncommonly associated with invasive aspergillosis. We describe herein the case of a young man, 34 years old, born to a non-consanguineous family, presenting chronic sinusitis treated with multiple antibiotic schemes for more than one year without resolution. He then presented tenderness in the frontal area of the head, fo llowed by ulceration. The computed tomography of brain showed osteolytic lesion of the skull, associated to invasion of the skin and paranasal sinuses. The biopsy showed fungal structures, identified as Aspergillus fumigatus. Laboratorial investigation evidenced normal blood cell counts, Ig levels, DHR, G6PD, myeloperoxidase and lymphocyte immunophenotyping. Lymphoproliferation assays showed decreased response to tetanus toxoid and toxoplasma, but normal response to CMV and T cell mitogens. Monocyte derived dendritic cells presented decreased activation parameters after Aspergillus as well as by Candida antigen stimulation. Ag specific T cell costimulation was also severely decreased when compared to healthy controls. This is to our knowledge the first case of a dendritic cell disturbance associated to invasive Aspergillus infection. This case report highlights the complex coordination of both innate and acquired pathways mediating host defense against Aspergillus infection.