Quinoline compounds decrease in vitro spontaneous proliferation of peripheral blood mononuclear cells (PBMC) from human T-cell lymphotropic virus (HTLV) type-1-infected patients

2008 ◽  
Vol 62 (7) ◽  
pp. 430-435 ◽  
Author(s):  
Fernanda Grassi ◽  
Ana Beatriz Guimarães Corrêa ◽  
Rita Elizabeth Mascarenhas ◽  
Bernardo Galvão ◽  
Blandine Séon-Méniel ◽  
...  
2002 ◽  
Vol 46 (9) ◽  
pp. 3080-3083 ◽  
Author(s):  
Emanuela Balestrieri ◽  
Giancarlo Forte ◽  
Claudia Matteucci ◽  
Antonio Mastino ◽  
Beatrice Macchi

ABSTRACT The effects of lamivudine (3TC) on in vitro infection of peripheral blood mononuclear cells (PBMC) from healthy donors with human T-cell lymphotropic virus type 1 (HTLV-1) were investigated. Direct measures of viral replication (viral DNA, RNA, and protein) all gave similar, very high 50% inhibitory concentrations in comparison with those previously reported for zidovudine. Nevertheless, 3TC inhibited HTLV-1-driven long-term growth of infected PBMC in vitro at concentrations (6.25 μM) which had poor or no direct antiviral effects, suggesting that another mechanism may be playing a role.


2006 ◽  
Vol 13 (5) ◽  
pp. 547-552 ◽  
Author(s):  
Rita Elizabeth Mascarenhas ◽  
Cláudia Brodskyn ◽  
Geisa Barbosa ◽  
Jorge Clarêncio ◽  
Antônio Souza Andrade-Filho ◽  
...  

ABSTRACT Evidence indicates that human T-cell lymphotropic virus type 1 (HTLV-1) infection leads to chronic immunosuppression and a greater susceptibility to infectious diseases. Spontaneous in vitro proliferation of peripheral blood mononuclear cells (PBMC) is an important immunological feature of HTLV-1-infected individuals. However, the association between spontaneous proliferation and immunosuppression is not clear. In this study, we evaluated the cellular immune responses of PBMC from 58 asymptomatic HTLV-1-infected individuals with PBMC showing or not showing spontaneous proliferation. Individuals with PBMC that spontaneously proliferated had increased proportions of CD4 T cells expressing CD45RO and dramatically reduced responses to recall antigens. In addition, frequencies of positive responses to recall antigens were also decreased in HTLV-infected individuals without spontaneous proliferation of PBMC. There was a polyclonal expansion of multiple T-cell receptor Vβ families of CD4+ T lymphocytes in patients with spontaneous proliferation. We observed that HTLV-1 induced an immunosuppression characterized by a decrease in the stimulation index to a recall antigen, even in individuals who did not present spontaneous proliferation. On the other hand, only patients with PBMC presenting spontaneous proliferation showed polyclonal activation and increased proportion of CD4 T cells expressing CD45RO.


2002 ◽  
Vol 83 (9) ◽  
pp. 2169-2176 ◽  
Author(s):  
Didier Hober ◽  
Wassim Chehadeh ◽  
Jacques Weill ◽  
Christine Hober ◽  
Marie-Christine Vantyghem ◽  
...  

Increased levels of IFN-α have been found in patients with type 1 diabetes who have detectable levels of coxsackievirus B4 (CVB4) RNA in their blood. The IFN-α-inducing activity of CVB4 in vitro is weak but can be enhanced by human IgGs. Therefore, it was investigated in vitro whether a preferential IFN-α response of peripheral blood mononuclear cells (PBMCs) to CVB4 exists in patients with type 1 diabetes (n=56) compared with healthy subjects (n=20) and whether antibodies play a role. In patients, the levels of IFN-α obtained after stimulation by PBMCs with CVB4 were higher (P=0·008), an individual IFN-α response by PBMCs to CVB4 was more frequent (P=0·0004) and increased levels of IFN-α were observed in CVB4-infected whole blood cultures. The IFN-α-inducing activity of patients plasma and IgGs mixed with CVB4 and then added to PBMCs was high in comparison with healthy subjects (P<0·001) and was inhibited by preincubating the cells with anti-FcγRII, anti-FcγRIII and anti-CAR (coxsackievirus and adenovirus receptor) antibodies. The strong IFN-α responsiveness of PBMCs to CVB4 suggested that IgGs bound to the cell surface might play a role. A short 56 °C incubation of PBMCs from patients responsive to CVB4 generated supernatants, which, when added to cells, exhibited IFN-α-enhancing activity in combination with CVB4, whereas those of controls did not. Specific antibodies for FcγRI, FcγRII and CAR inhibited this activity. These studies demonstrate that CVB4, through interactions with circulating and/or cell-bound IgGs, can strongly induce the production of IFN-α by PBMCs from patients with type 1 diabetes.


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