Cellular immune response to specific and non-specific stimulants was investigated, both in vivo and in vitro, in 29 healthy controls and in 53 previously untreated patients with the chronic isolated organic form (CIOF), the chronic mixed form (CMF) and the acute progressive form (APF) of paracoccidioidomycosis. The study included skin tests to Paracoccidioides brasiliensis antigen (PbAg) and phytohaemagglutinin (PHA), DNCB sensitization, determination of T lymphocytes and complement rosette-forming cells, lymphocyte transformation and leucocyte migration inhibition tests using PbAg and PHA. Patients displayed staggered cutaneous response to PHA and to PbAg, with marked decrease in intensity in the APF group. DNCB sensitization test and proliferative response of lymphocytes to PHA and PbAg were severely depressed in most of the patients. Leucocyte migration inhibition indices to PbAg were highly positive, while response to PHA was slightly decreased regardless of the clinical form. The number of T lymphocytes was reduced in most of patients and in them the number of complement-rosette forming cells was normal. The distribution of patients according to a suppression index, based in the results of the tests employed, revealed a tendency towards an increased degree of cellular immunosuppression from the least severe (CIOF) to the most severe (APF) clinical form of the disease. On the whole, the present study demonstrated a gamut of immunological reactivity in paracoccidioidomycosis.

The present paper describes a murine model for pulmonary paracoccidioidomycosis injecting 6 X 10(5) yeast forms of Paracoccidioides brasiliensis (Pb) by the direct intratracheal route. The sequential histopathology of lung and dissemination lesions together with humoral (immunodiffusion test) and cellular immune response (footpad test and macrophage inhibition factor assay - MIF assay) were investigated since the 1st to the 360th day after infection. All infected animal showed pulmonary Pbmycosis up to Day 30; onwards the lesions subsided being found only in one mouse at Day 360. Dissemination lesions were observed in paratracheal and cervical lymph nodes in 9 out of 68 infected animals. Histologically early lesions were rich in polymorphonuclear cells and evolved to a macrophage desquamative pneumonitis at Day 15 and to typical epithelioid granulomata from Day 30 up to Day 360. Specific precipitating antibodies were first detected 15 days after infection, peaked from Day 30 to 60 and were not observed at Day 360. Significant cell-mediated immunity to Pb was noted at Day 15 with the peak reaction at Day 60 and 90. The intratracheal route represents a highly effective way of infecting mouse with Pb. This experimental pulmonary Pbmycosis is a granulomatous inflammation which courses with specific humoral and cellular immune response. It may be a good tool for further investigation in the pathogenesis and natural history of the disease.

Seventy untreated paracoccidioidomycosis patients, 15 with the acute or subacute form of the disease and 55 with the chronic form, were compared with two normal control groups of the same age range. Peripheral blood mononuclear cell subsets were defined by monoclonal antibodies directed at total T cells, helper/inducer and suppressor/cytotoxic T cell subpopulations; B cells, conical thymocytes and monocyte/null cells. Both groups of patients showed an increased number of monocyte/null cells, a low helper/suppressor ratio and a reduced percentage of total T cells and their helper/inducer subsets. In addition patients with the acute form of the disease exhibited high levels of suppressor/cytotoxic T cells and B cells. These findings are of importance in our attempts to understand the pathogenesis of this mycosis and also to evaluate its prognosis in individual patients.Paracoccidioidomycosis, a chronic granulomatous disease caused by the dimorphic fungus Paracoccidioides brasiliensis, is the most prevalent human systemic mycosis in Latin America. The disease may be classified into three clinical forms: (i) the acute or subacute form, with intense involvement of the mononuclear phagocyte system which affects young people, (ii) the chronic form, with an insidious evolution and involvement of one or more organs or systems, which generally affects adult males and (iii) the residual sequelar form, with manifestations related to cicatrization of old lesions [14].

It is proposed thatIn this context, the present work was carried out in order to investigate humoral and cellular immune response to brain tissues, in children with West syndrome and its related condidion, the Lennox-Gastaut syndrome. MATERIAL AND METHODSThe test group consisted of 24 children, aged between 4 months and 18 years, whose clinical and eletroencephalographic (EEG) features allowed the diagnosis of West and Lennox-Gastaut syndromes. Twenty healthy children, 12 male and 8 female (age range, 6 months to 8 years) formed the control group. Remarkable clinical characteristics and EEG alterations at the moment of immunological evaluation are detailed in table 1.