title: Anti-idiotypic antibodies in patients with different clinical forms of paracoccidioidomycosis.
abstract: Paracoccidioidomycosis (PCM) is the most prevalent systemic mycosis in Latin America. Patients with PCM show a wide spectrum of clinical and pathological manifestations depending on both host and pathogen factors. Two clinical forms of the disease are recognized: the acute or juvenile form and the chronic or adult form. The major antigenic component of the parasite is a glycoprotein of 43 kDa (gp43). All patient sera present antibodies against gp43 (anti-gp43) and, as demonstrated before by our group, spontaneous anti-idiotypic (anti-Id) antibodies (Ab2) can be detected in patient sera with high titers of anti-gp43. Since it has been postulated that anti-Id antibodies may have a modulating function, we decided to purify and characterize anti-Id antibodies in this system. The possible correlation of Ab2 titers with different clinical forms of disease was also verified. Results showed that purified human anti-Id antibodies (human Ab2) recognized specifically the idiotype of some murine monoclonal anti-gp43 (17c and 3e) but not others (40.d7, 27a, and 8a). Spontaneous anti-Id antibodies were found in all clinical forms of disease. The majority of patients (88%, n = 8) with the acute form of PCM had high titers of Ab2. However, among patients with the multifocal chronic form of the disease, only 29% (n = 14) had high titers of Ab2; 70% (n = 10) of patients with the unifocal chronic form had low titers of Ab2. A correlation between Ab2 titers and anti-gp43 titers was observed before and during antimycotic treatment. Our results suggest that titers of anti-Id antibodies correlate with the severity of PCM in humans.
authors.affiliation: Discipline of Immunology, Federal University of São Paulo (UNIFESP), São Paulo Brazil.
authors.forename: A R
authors.initials: AR
authors.lastname: Souza
authors.forename: J L
authors.initials: JL
authors.lastname: Gesztesi
authors.forename: G M
authors.initials: GM
authors.lastname: del Negro
authors.forename: G
authors.initials: G
authors.lastname: Benard
authors.forename: J
authors.initials: J
authors.lastname: Sato
authors.forename: M V
authors.initials: MV
authors.lastname: Santos
authors.forename: T B
authors.initials: TB
authors.lastname: Abrahão
authors.forename: J D
authors.initials: JD
authors.lastname: Lopes
mesh_terms: D000328:Adult; D000818:Animals; D000888:Antibodies, Anti-Idiotypic / Q000097:blood / Q000276:immunology* / Q000302:isolation & purification; D000908:Antibodies, Fungal / Q000097:blood / Q000276:immunology* / Q000302:isolation & purification; D000911:Antibodies, Monoclonal / Q000276:immunology / Q000302:isolation & purification; D000935:Antifungal Agents / Q000627:therapeutic use; D000946:Antigens, Fungal; D015725:Fluconazole / Q000627:therapeutic use; D005500:Follow-Up Studies; D005656:Fungal Proteins; D006023:Glycoproteins / Q000276:immunology*; D006801:Humans; D017964:Itraconazole / Q000627:therapeutic use; D051379:Mice; D009844:Oligosaccharides / Q000276:immunology*; D010228:Paracoccidioides / Q000276:immunology; D010229:Paracoccidioidomycosis / Q000097:blood / Q000188:drug therapy / Q000276:immunology* / Q000503:physiopathology
chemical_list: C103180:43 kDa protein, Paracoccidioides; D000888:Antibodies, Anti-Idiotypic; D000908:Antibodies, Fungal; D000911:Antibodies, Monoclonal; D000935:Antifungal Agents; D000946:Antigens, Fungal; D005656:Fungal Proteins; D006023:Glycoproteins; D009844:Oligosaccharides; D017964:Itraconazole; D015725:Fluconazole