ANTIGEN-SPECIFIC IMMUNOSUPPRESSION IN PARACOCCIDIOIDOMYCOSIS

Citation
G. Benard et al., ANTIGEN-SPECIFIC IMMUNOSUPPRESSION IN PARACOCCIDIOIDOMYCOSIS, The American journal of tropical medicine and hygiene, 54(1), 1996, pp. 7-12
Citations number
23
Categorie Soggetti
Public, Environmental & Occupation Heath","Tropical Medicine
ISSN journal
00029637
Volume
54
Issue
1
Year of publication
1996
Pages
7 - 12
Database
ISI
SICI code
0002-9637(1996)54:1<7:AIIP>2.0.ZU;2-U
Abstract
To characterize the immune dysfunction associated with paracoccidioido mycosis, we studied the in vitro lymphocyte reactivity to phytohemaggl utinin (PHA), pokeweed mitogen (PWM), a Candida albicans antigen (CMA) , and a Paracoccidioides brasiliensis antigen (PbAg) in 32 patients wi th the acute and the chronic form of the disease before or during the initial phase of treatment and after clinical cure. We also studied, a s controls, 30 healthy individuals, 15 of them immune to P. brasiliens is. Results showed a strong hyporesponsiveness to the PbAg while respo nses to mitogens and CMA were comparable with those of controls. Patie nts with the acute form of the disease (usually more severe) had more marked PbAg hyporesponsiveness than those with the chronic form. After patients' clinical cure, PbAg proliferative responses were similar to controls and greater than those seen before pretreatment. Changes in other parameters were also seen in the treated patients: skin test ane rgy to paracoccidioidin, high levels of anti-P. brasiliensis antibodie s, leukocytosis, and eosinophilia. These changes were usually more int ense in patients with the acute form of the disease. The post-treatmen t CD4+, CD8+, and total lymphocyte counts were similar to those of con trols. Correlation between these parameters and the lymphoproliferativ e responses to the various stimuli was only found with PbAg: PbAg resp onses correlated inversely with eosinophil and anti-P. brasiliensis an tibody levels. Overall, our results demonstrate an antigen-specific ce llular immunity defect, which is reversible with treatment and possibl y related to a T helper cell-2 pattern of immune response during activ e disease.