Macrophage deactivation by interleukin 10.

Bogdan, Christian; Vodovotz, Yoram; Nathan, C F

doi:10.1084/jem.174.6.1549

Cited by 1,152 publications

(658 citation statements)

References 41 publications

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“…The amount of NO produced by the METH extract (105.99 µmol/5 × 10 5 cells) was larger than the production of the DCM extract (58.9 µmol/5 × 10 5 cells) (Figure 1). The results regarding TNF-α confirmed a significant production of this cytokine, at levels near that of the positive control (252.7 and 234.6 units/ mL, METH and DCM extracts, respectively), confirming a correlation between the synthesis of TNF-α and NO (Figure 2) (Bogdan et al, 1991;Carli et al, 2009). I. suffruticosa did not produce significant amounts of H 2 O 2 when compared with the negative control (p > 0.05): METH, 0.59 nmol/2 × 10 5 cells and DCM, 3.3 nmol/2 × 10 5 cells) (Figure 3).…”

Section: Resultssupporting

confidence: 59%

Antimycobacterial activity ofIndigofera suffruticosawith activation potential of the innate immune system

Carli¹,

Quilles²,

Maia³

et al. 2010

Pharmaceutical Biology

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Section: Resultssupporting

confidence: 59%

Antimycobacterial activity ofIndigofera suffruticosawith activation potential of the innate immune system

Carli¹,

Quilles²,

Maia³

et al. 2010

Pharmaceutical Biology

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“…The IL-10 activity minimizes the tissular impairment occurred in the disease's site through inhibiting the production of proinflammatory cytokines (Bogdan et al 1991, D'Andrea et al 1993. In this study, PBMCs of patients with active pulmonary TB were observed to produce high levels of IL-10.…”

Section: Discussionmentioning

confidence: 79%

Pulmonary tuberculosis: evaluation of interferon-gamma levels as an immunological healing marker based on the response to the Bacillus Calmette-Guerin

Moura¹,

Toledo²,

Oliveira

et al. 2004

Mem. Inst. Oswaldo Cruz

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Tuberculosis (TB) is a disease caused by Mycobacterium tuberculosis whose interaction with the host may lead to a cell-mediated protective immune response. The presence of interferon-γ (IFN-γ) is related to this response. With the purpose of understanding the immunological mechanisms involved in this protection, the lymphoproliferative response, IFN-γ and other cytokines like interleukin , and tumor necrosis factor alpha (TNF-α) Key words: tuberculosis -interleukin-5 -interleukin-10 -tumor necrosis factor alpha -interferon-γ -peripheral blood mononuclear cells Tuberculosis (TB), a chronic infective-contagious disease, is caused by Mycobacterium tuberculosis and remains an important public health problem whose mechanisms related to a protective immunity in humans are not clear. The resurgence of TB has stimulated studies for the development of vaccines, new diagnostic methods and less toxic and more effective drugs for treatment (Laal et al. 1997). The cellular immunity plays an important role in TB healing (Ladel et al. 1997, Torres et al. 1998, Turner et al. 2000, Chackerian et al. 2001). Resistance to mycobacterial infections is conferred by immunological mechanisms mediated by T CD4 + lymphocytes, involving cytokines that increase the microbicide activity of macrophages (Dlugovitzky et al. 2000, Oberholzer et al. 2000. Studies in murine and human models allow differentiating two subpopulations of T CD4 + lymphocytes termed Th1 and Th2, that mediate the protection or the aggravation of the disease (Ladel et al. 1997, Kori et al. 2000. This existing dichotomy between the protective or non-protective immune responses is likely to be correlated with cytokine patterns produced by different subpopulations of lymphocytes during initial surviving stages of the pathogens inside macrophages. Interferon-γ (IFN- γ) acts as a powerful macrophage activator, increasing the molecule expression of the main class II histocompatibility complex and the potentialization of the cell response, including the production of cytokines, nitric oxide, and the increase of the cytolitic activity, with a main role in the Th1 type (Flesh et al. 1995). Studies carried out by Cooper et al. (1993) and Flynn et al. (1993) demonstrated that mice without the IFN-γ gene were not able to fight off the infection caused by M. tuberculosis. In humans, individuals who presented genetic mutations in the receptors for IFN-γ were observed to have had a high susceptibility to acquire infections caused by atypical mycobacteria (Jouanguy et al. 1996), suggesting an important role of IFN-γ in the protective response against TB.Besides the importance of better understanding the immunological mechanisms that may contribute to the healing, it becomes essential to determine markers of healing lesions, once this is currently carried out based on the clinical, radiological, and negative bacterioscopy.In this work, we proposed the in vitro evaluation of IFN-γ levels produced by peripheral blood mononuclear cells (PBMC) after Bacillus Calmette-Guerin (BCG) stimulati...

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“…9, 41 We believe that vIL-10 not only deactivates macrophages via the prevention of IFN-g production by Th1 cells, but also deactivates macrophages directly, and inhibits the production of TNF-a by macrophages. MCP-1 is released from many types of cells, including macrophages, lymphocytes, platelets, fibroblasts, endothelial cells, epithelial cells, 42 and mesangial cells.…”

Section: Discussionmentioning

confidence: 99%

Hydrodynamics-based delivery of the viral interleukin-10 gene suppresses experimental crescentic glomerulonephritis in Wistar–Kyoto rats

et al. 2003

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Gene therapy is expected to revolutionize the treatment of kidney diseases. Viral interleukin (vIL)-10 has a variety of immunomodulatory properties. We examined the applicability of vIL-10 gene transfer to the treatment of rats with crescentic glomerulonephritis, a T helper 1 (Th 1) predominant disease. To produce the disease, Wistar-Kyoto rats were injected with a rabbit polyclonal anti-rat glomerular basement membrane antibody. After 3 h, a large volume of plasmid DNA expressing vIL-10 (pCAGGS-vIL-10) solution was rapidly injected into the tail vein. pCAGGS solution was similarly injected into control rats (pCAGGS rats). We confirmed the presence of vector-derived vIL-10 mainly in the liver and observed high serum vIL-10 levels in pCAGGSvIL-10-injected rats. Compared with the pCAGGS rats, the pCAGGS-vIL-10 rats showed significant therapeutic effects: reduced frequency of crescent formation, decrease in the number of total cells, macrophages, and CD4 + T cells in the glomeruli, decrease in urine protein, and attenuation of kidney dysfunction. Using quantitative real-time polymerase chain reaction, we also observed that this model was Th1-predominant in the glomeruli and that the ratio of the transcripts of CD4, interferon-g, tumor necrosis factor-a, and monocyte chemotactic protein-1 to the transcripts of glucose-6-phosphate dehydrogenase in the glomeruli were all significantly lower in the pCAGGS-vIL-10 rats than in the pCAGGS rats. These results demonstrate that pCAGGS-vIL-10 gene transfer by hydrodynamics-based transfection suppresses crescentic glomerulonephritis.

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Macrophage deactivation by interleukin 10.

Cited by 1,152 publications

References 41 publications

Antimycobacterial activity ofIndigofera suffruticosawith activation potential of the innate immune system

Antimycobacterial activity ofIndigofera suffruticosawith activation potential of the innate immune system

Pulmonary tuberculosis: evaluation of interferon-gamma levels as an immunological healing marker based on the response to the Bacillus Calmette-Guerin

Hydrodynamics-based delivery of the viral interleukin-10 gene suppresses experimental crescentic glomerulonephritis in Wistar–Kyoto rats

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