Fonsecaea pedrosoi infection induces differential modulation of costimulatory molecules and cytokines in monocytes from patients with severe and mild forms of chromoblastomycosis.
The host defense mechanism in chromoblastomycosis has not been thoroughly investigated. It has been suggested that cell-mediated immunity in patients with long-standing chromoblastomycosis is somehow impaired. As a result, these individuals became unable to develop an efficient immune reaction. Many studies have shown that monocyte-derived macrophages exhibit critical activities in immunity to microorganisms. Moreover, the ability of cells from the monocytic lineage to process and present antigens, to produce cytokines, and to provide costimulatory signals confirms their pivotal role in the initiation of specific immune responses. In the present study, it was observed that monocytes from patients with a severe form of disease had a higher production of IL-10 and a lower expression of HLA-DR and costimulatory molecules when stimulated with specific antigen or LPS. Immune modulation with recombinant IL-12 or anti-IL-10 can restore the antigen-specific Th1-type immune response in chromoblastomycosis patients by up-regulating HLA-DR and costimulatory molecules in monocytes. Therefore, our data show that monocytes from patients with different clinical forms of chromoblastomycosis present distinct phenotypic and functional profiles. This observation suggests possible mechanisms that control the T cell response and influence their role in the development of pathology.
Sousa
Maria Glória Teixeira
MG
Departamento de Análises Clínicas e Toxicológicas, Faculdade de Ciências Farmacêuticas, Universidade de São Paulo, São Paulo, SP, Brazil.
de Maria Pedrozo e Silva Azevedo
Conceição
C
Nascimento
Rosana Cicera
RC
Ghosn
Eliver Eid Bou
EE
Santiago
Karla Leticia
KL
Noal
Vanessa
V
Bomfim
Gisele Facholi
GF
Marques
Sirlei Garcia
SG
Gonçalves
Azizedite Guedes
AG
Wagner de Castro Lima Santos
Daniel
D
Almeida
Sandro Rogerio
SR
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015703:Antigens, CD; D001203:Ascomycota / Q000302:isolation & purification* / Q000472:pathogenicity; D018122:B7-1 Antigen / Q000276:immunology / Q000378:metabolism; D060908:CTLA-4 Antigen; D002450:Cell Communication / Q000276:immunology; D049109:Cell Proliferation; D002862:Chromoblastomycosis / Q000276:immunology* / Q000378:metabolism* / Q000382:microbiology; D016207:Cytokines / Q000276:immunology / Q000378:metabolism*; D005260:Female; D006684:HLA-DR Antigens / Q000276:immunology / Q000378:metabolism; D006801:Humans; D016753:Interleukin-10 / Q000276:immunology / Q000378:metabolism; D018664:Interleukin-12 / Q000276:immunology / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology; D008213:Lymphocyte Activation / Q000276:immunology; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology* / Q000378:metabolism* / Q000382:microbiology; D013601:T-Lymphocytes / Q000276:immunology / Q000378:metabolism / Q000382:microbiology; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology / Q000378:metabolism
D015703:Antigens, CD; D018122:B7-1 Antigen; D060908:CTLA-4 Antigen; C556706:CTLA4 protein, human; D016207:Cytokines; D006684:HLA-DR Antigens; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D018664:Interleukin-12