Modulation of CD28 and CD86 Expression in Patients with Paracoccidioidomycosis in Different Periods of Treatment

Abstract

Paracoccidioides brasiliensis, a thermo-dimorphic fungus, is the ethiologic agent of paracoccidioidomycosis (PCM). The recidive is the greatest obstacle of this disease, because the yeast usually returns after the long treatment period. In the present work, we have investigated the cellular immune response of cells from peripheral blood drawn from patients with different duration of PCM. The classification of patients ranged from nontreated to those with long-standing disease over 5 years. Unstimulated as well as cells stimulated with phytohemaglutinin or two different antigen preparations, secreted (MEXO) or somatic (PbAg) of P. brasiliensis, were characterized. We found that cells from patients with disease proliferate considerably upon stimulation with the antigen preparations and that cells from patients with disease of long duration does not proliferate that vigorously as from patients with more recent diagnosis. Both interferon (IFN)-gamma and interleukin (IL)-4 appear to be increased in patients, but IFN-gamma tended to increase upon treatment while IL-4-secretion decreased. With respect to CD28 and CD86, we found that the subset of CD28 positive CD8 cells are decreased in all stages of the disease as compared to control individuals. A subset of CD86 positive CD19 cells appeared to be considerably increased compared to the controls. Indeed, our results demonstrated that the treatment of PCM patients promoted a regulation of IFN-gamma, IL-4 levels and CD28, CD86 expression bringing new insight to the cellular immune response in PCM.

Patients referred to an indoor air health clinic: exposure to water-damaged buildings causes an increase of lymphocytes in bronchoalveolar lavage and a decrease of CD19 leucocytes in peripheral blood

“…The CD19 molecule is thought to regulate signalling by the toll-like receptor RP 105 [26]. CD19 ϩ CD86ϩ cells have been reported to increase in patients with the fungal disease paracoccidomycosis [27]. Resistance to treatment for the dermatophyte onchomycosis has been associated with low levels of blood CD19-positive cells [28].…”

Polymorphism analysis of the CTLA-4 gene in paracoccidioidomycosis patients

“…Although some studies have been published concerning the influence of CTLA-4 on PCM (Bozzi et al 2004, Cavassani et al 2006, this study is the first to assess the association of polymorphisms and the fungal illness. Notably, population and individual genetic structure analysis was carried out on the patient and control groups.…”

Paracoccidioidomycosis disease (Lutz-Splendore-Almeida): etiology, epidemiology, and pathogenesis

“…The process is followed by lymphatic spread with lymphangitis and regional Paracoccidioidomycosis disease (Lutz-Splendore-Almeida): etiology, epidemiology, and pathogenesis gens, located in the infectious focus, are initially recognized by macrophages and dendritic cells, which activate the complement system, release cytokines, and promote the chemotaxis of neutrophils circulating toward this focus; and with the evolution of inflammatory processes, are replaced by mononuclear cells. [33][34][35][36][37][38] Neutrophils and macrophages, once reaching the infectious focus, cannot digest the fungus and prevent its multiplication, however, they are able to promote fungal debugging if they are activated by interferongamma (IFN-γ) and alpha tumor necrosis factor (TNF-α). TNF-α is able to activate T lymphocytes (L); and IFN-γ, through NK cells and LTCD4 + , activates macrophages, which results in the inhibition of P. brasiliensis replication.…”

“…The repressed response of LTh1 promotes the decrease of LT, NK cells activity, production of INF-γ, TNF-α, and IL-2 (and its receptor), and consequent decreased proliferative response from lymphocytes, favoring the establishment of the PCM-disease. [33][34][35][36][37][38]…”