ÿþ<HTML><HEAD><TITLE>XI International Meeting on Paracoccidioidomycosis</TITLE><link rel=STYLESHEET type=text/css href=css.css></HEAD><BODY aLink=#ff0000 bgColor=#FFFFFF leftMargin=0 link=#000000 text=#000000 topMargin=0 vLink=#000000 marginheight=0 marginwidth=0><table align=center width=700 cellpadding=0 cellspacing=0><tr><td align=left bgcolor=#cccccc valign=top width=550><font face=arial size=2><strong><font face=Verdana, Arial, Helvetica, sans-serif size=3><font size=1>XI International Meeting on Paracoccidioidomycosis</font></font></strong><font face=Verdana size=1><b><br></b></font><font face=Verdana, Arial,Helvetica, sans-serif size=1><strong> </strong></font></font></td><td align=right bgcolor=#cccccc valign=top width=150><font face=arial size=2><strong><font face=Verdana, Arial, Helvetica, sans-serif size=1><font size=1>Resume:108-1</font></em></font></strong></font></td></tr><tr><td colspan=2><br><br><table align=center width=700><tr><td><b>Oral / Poster</b><br><table width="100%"><tr><td width="60">108-1</td><td><b>DIFFERENT PATTERNS OF CYTOKINE PRODUCTION AND CELLULAR INFILTRATES DISTINGUISH CLINICAL FORMS OF HUMAN PARACOCCIDIOIDOMYCOSIS</b></td></tr><tr><td valign=top>Authors:</td><td><u>Rosiane Maria Silva </u> (UNICAMP - Universidade Estadual de Campinas) ; Ronei Luciano Mamoni (UNICAMP - Universidade Estadual de Campinas) ; Maria Cecilia Ferro (PUCSP - Pontificia Universidade Catolica de Sao Paulo) ; Albina Altemani (UNICAMP - Universidade Estadual de Campinas) ; Maria Heloisa Souza Lima Blotta (UNICAMP - Universidade Estadual de Campinas) </td></tr></table><p align=justify><b><font size=2>Abstract</font></b><p align=justify class=tres><font size=2>Introduction and Aims: Paracoccidioidomycosis (PCM), a disease caused by the dimorphic fungus P. brasiliensis, presents with a wide spectrum of clinical and immunological manifestations, varying from benign and localized forms to severe and disseminated forms. The chronic or adult form (AF) is characterized by localized lesions with involvement of the skin, oral mucosa (OM) and pulmonary nodules; the acute or juvenile form (JF) is more severe with the involvement of the liver, spleen and lymph nodes (LN). In order to examine the immune response in the lesions from patients with PCM, we analyzed the expression of cytokines and the phenotype of the cellular infiltrate. Material and Methods: Paraffin-embedded OM and LN biopsies from 30 patients of PCM were analyzed by immunohistochemistry. We characterized the cellular infiltrate (CD3, CD8, CD15, CD68 and FOXp3) and cytokines (IL-10, IL-12, IL-17, IL-18, IL-23, IFN-&#61543;). Results and Conclusions: Most of the inflammatory cells in the LN were CD68+ (macrophages and giant cells), while a mixed infiltrate composed by CD68+ and neutrophils (CD15+) was detected in the OM. Lymphocytes (CD3+ and CD8+) were detected in large amounts in both clinical forms of the disease. IL-12+ macrophages were very scarce and IFN-&#61543;+ lymphocytes, IL-17+ and IL-23+ cells were detected mainly in OM than in LN. We found an elevated number of Foxp3+ cells in OM, but not in LN. These results suggest that the local production of cytokines may account to the differential immune response that characterizes the clinical forms of PCM. Exacerbated inflammatory reaction in lesions without the control of Treg (Foxp3+) could lead to a deficient control of fungal growth in the lesions of the JF of the disease. On the other hand, in the patients with AF, the production of the cytokines IFN-&#947;, IL-12 and IL-17, with the presence of CD15+and the Treg could result in an improved control of fungal growth and a more efficient immune response. Financial support: FAPESP and CNPq </font></p><br><b>Keyword: </b>&nbsp;PARACOCCIDIOIDOMYCOSIS, CITOKINES, IMMUNOHISTOCHEMISTRY</td></tr></table></tr></td></table></body></html>