CD80+Gr-1+ Myeloid Cells Inhibit Development of Antifungal Th1 Immunity in Mice with Candidiasis
| Autor: | Claudia Montagnoli, Elio Cenci, Antonio Spreca, Antonella Mencacci, Arlene H. Sharpe, Lucia Pitzurra, Luigina Romani, Angela Bacci, Manfred Kopf |
|---|---|
| Rok vydání: | 2002 |
| Předmět: |
CD4-Positive T-Lymphocytes
Neutrophils medicine.medical_treatment Immunology Population Antigens Differentiation Myelomonocytic Biology Lymphocyte Activation Nitric Oxide T-Lymphocytes Regulatory Immune tolerance Microbiology Interferon-gamma Mice CD28 Antigens Antigen In vivo Candida albicans Immune Tolerance medicine Animals Humans Immunology and Allergy Myeloid Cells education Cells Cultured Mice Knockout CD86 Mice Inbred BALB C Mice Inbred C3H education.field_of_study Candidiasis hemic and immune systems Th1 Cells Immunity Innate In vitro Interleukin-10 Mice Inbred C57BL Cytokine B7-1 Antigen Cytokines Female Cell Division CD80 |
| Zdroj: | Scopus-Elsevier |
| ISSN: | 1550-6606 0022-1767 |
| DOI: | 10.4049/jimmunol.169.6.3180 |
| Popis: | To find out whether polymorphonuclear neutrophils (PMN), abundantly recruited in disseminated Candida albicans infection, could directly affect the activation of Th cells we addressed the issues as to whether murine PMN, like their human counterparts, express costimulatory molecules and the functional consequence of this expression in terms of antifungal immune resistance. To this purpose, we assessed 1) the expression of CD80 (B7-1) and CD86 (B7-2) molecules on peripheral, splenic, and inflammatory murine Gr-1+ PMN; 2) its modulation upon interaction with C. albicans in vitro, in vivo, and in human PMN; 3) the effect of Candida exposure on the ability of murine PMN to affect CD4+ Th1 cell proliferation and cytokine production; and 4) the mechanism responsible for this effect. Murine PMN constitutively expressed CD80 molecules on both the surface and intracellularly; however, in both murine and human PMN, CD80 expression was differentially modulated upon interaction with Candida yeasts or hyphae in vitro as well as in infected mice. The expression of the CD86 molecule was neither constitutive nor inducible upon exposure to the fungus. In vitro, Gr-1+ PMN were found to inhibit the activation of IFN-γ-producing CD4+ T cells and to induce apoptosis through a CD80/CD28-dependent mechanism. A population of CD80+Gr-1+ myeloid cells was found to be expanded in conventional as well as in bone marrow-transplanted mice with disseminated candidiasis, but its depletion increased the IFN-γ-mediated antifungal resistance. These data indicate that alternatively activated PMN expressing CD80 may adversely affect Th1-dependent resistance in fungal infections. |
| Databáze: | OpenAIRE |
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