Evaluation of IFN-gamma and TNF-alpha as immunological markers of clinical outcome in cutaneous leishmaniasis

Júnior, Argemiro D’Oliveira; Machado, Paulo Roberto Lima; Bacellar, Olı́via; Cheng, Lay Har; Almeida, Roque Pacheco de; Carvalho, Edgar M.

doi:10.1590/s0037-86822002000100002

Cited by 25 publications

(11 citation statements)

References 13 publications

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“…The immune response of the New World LCL caused by L. braziliensis, is characterized by a Th1 response, with a predominance of IFN-gamma expression in vitro and in situ and a very low or sometimes absent expression of IL-4, IL-5 and IL-10 1,2,5, [11][12][13][14][15]20 . In relation to other cytokines, such as IL-2, they have been demonstrated in vitro and in situ, with a low expression.…”

Section: Discussionmentioning

confidence: 99%

Cytokine profile in Montenegro skin test of patients with localized cutaneous and mucocutaneous leishmaniasis

Nogueira

Goto

Sotto

et al. 2008

Rev. Inst. Med. trop. S. Paulo

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SuMMarYAmerican tegumentary leishmaniasis presents as two major clinical forms: localized cutaneous leishmaniasis (LCL) and mucocutaneous leishmaniasis (MCL). The immune response in leishmaniasis is efficiently evaluated by the response to Leishmania antigen through the Montenegro skin test (MST). Both LCL and MCL present positive response to MST, indicating that the patients present cell-mediated immunity against the parasite -Leishmania. In spite of the presence of immunity in MCL, this is not sufficient to stop disease progression and prevent resistance to treatment. In this study we demonstrated interleukin (IL) 2, 4, 5 and interferon (IFN) gamma expression in biopsies of MST of ten patients with American tegumentary leishmaniasis. The obtained results were compared between LCL (n = 5) and MCL (n = 5) patients. The MST of MCL patients displayed a higher expression of IL-2, IL-4 and IL-5, in comparison to LCL. There was no significant difference in IFN-gamma expression between groups. The obtained results suggest the role of IL-4 and IL-5 in the maintenance of the immunopathogenic mechanism of the destructive lesions that characterize MCL.

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Section: Discussionmentioning

confidence: 99%

Cytokine profile in Montenegro skin test of patients with localized cutaneous and mucocutaneous leishmaniasis

Nogueira

Goto

Sotto

et al. 2008

Rev. Inst. Med. trop. S. Paulo

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“…The role of a number of immune system productions, such as pro‐inflammatory cytokine TNF‐α, IL‐17 and IL‐22 in CL outcome, needs more clarification. Existing data on the role of TNF‐α in human leishmaniasis development are controversial, but most of the reports implicate that unregulated production of TNF‐α may contribute to the clinical outcome of leishmaniasis early at infection . It was reported that percentage of Leishmania ‐specific TNF‐α‐producing T cells has a positive correlation with the lesion size and elevated levels of TNF‐α production were shown in lesions of CL patients nonresponsive to antimonial treatment .…”

Section: Introductionmentioning

confidence: 99%

Tumour Necrosis Factor‐alpha (TNF‐α) and its soluble receptor type 1 (sTNFR I) in human active and healed leishmaniases

Rostami

Jasbi

Khamesipour

2016

Parasite Immunology

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The role of tumour necrosis factor-alpha (TNF-α) is not fully understood in human leishmaniasis. We analysed the alterations in the levels of TNF-α, soluble TNF receptor type 1 (sTNFR I), IL-17 and IL-22 productions in active and healed leishmaniases. Blood samples were collected from volunteers with active cutaneous leishmaniasis (ACL), the same subjects after lesion healing (healed CL = HCL), volunteers with active visceral leishmaniasis (AVL), healed VL (HVL) and healthy controls. Levels of cytokines were titrated on Leishmania Ag-stimulated PBMC culture. The mean level of TNF-α production from stimulated cells was significantly higher in ACL than controls (P < 0·001) and significantly reduced after treatment in HCL volunteers (P < 0·05). The mean level of sTNFR I production was significantly higher in ACL than controls (P < 0·001) and significantly reduced after treatment in HCL volunteers (P < 0·05). The mean level of IL-22 production in AVL was significantly higher than controls (P < 0·05) and was significantly lower in HVL compared with AVL (P < 0·001) and controls (P < 0·05). The levels of TNF-α (P = 0·0025) and sTNFR I (P < 0·01) productions from PBMCs showed significant decreasing trend after treatment in each CL volunteer. Reduction in TNF-α is associated with clinical response to treatment and healing of CL lesions due to L. major.

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“…However, peripheral blood mononuclear cells (PBMC) from both CL and ML patients produce high amounts of IFN‐γ and TNF‐α when stimulated with soluble leishmania antigen (SLA) [6], and evidence has been accumulating that tissue damage in these diseases may be due to the host immune response [6–8]. For instance, (1) treatment with antimony of early cutaneous lesions does not prevent the development of ulcers [9]; (2) SLA‐stimulated PBMC from ML patients produce higher levels of IFN‐γ and TNF‐α and lower levels of IL‐10 than PBMC from CL patients [6]; (3) IFN‐γ and TNF‐a levels fall after successful antimony therapy [10, 11] and (4) drugs that down modulate the immune response combined with antimony increase the cure rate and decrease the healing time of mucosal lesions [8].…”

Section: Introductionmentioning

confidence: 99%

Effect of LACK and KMP11 on IFN‐γ Production by Peripheral Blood Mononuclear Cells from Cutaneous and Mucosal Leishmaniasis Patients

et al. 2005

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The immune modulatory properties of recombinant antigens Kinetoplasmid membrane protein-11 (KMP11) and Leishmania homologue of receptors for activated C kinase (LACK) in cutaneous leishmaniasis (CL) and mucosal leishmaniasis (ML) patients were evaluated. The mean levels of interferon-g (IFN-g) in soluble leishmania antigen (SLA) stimulated peripheral blood mononuclear cells (PBMC) of ML and CL patients were 5625 AE 2333 pg/ml and 4422 AE 3665 pg/ml, respectively. IFN-g was not detected in cultures stimulated with KMP11 or LACK. Interleukin-10 (IL-10) concentration in SLA, KMP11 and LACK-stimulated PBMC of ML patients was 13 AE 12 pg/ml, 285 AE 388 pg/ml and 802 AE 483 pg/ml, respectively. Addition of KMP11 or LACK to SLAstimulated PBMC of CL and ML patients enhanced IL-10 production (P < 0.05). Addition of KMP11 decreased IFN-g levels by 52% in CL patients and by 19% in ML patients. Addition of LACK to SLA-stimulated cultures decreased IFN-g levels by 58% in CL patients and by 30% in ML patients. Neutralization of IL-10 abrogated the downregulatory effect of LACK and KMP11. The modulatory properties of LACK and KMP11 are due to induction of IL-10 production and may be helpful for attenuating chronic inflammatory diseases. However, in some clinical conditions, as demonstrated for ML, these molecules are not able to suppress the IFN-g response, even inducing IL-10 production.

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Evaluation of IFN-gamma and TNF-alpha as immunological markers of clinical outcome in cutaneous leishmaniasis

Cited by 25 publications

References 13 publications

Cytokine profile in Montenegro skin test of patients with localized cutaneous and mucocutaneous leishmaniasis

Cytokine profile in Montenegro skin test of patients with localized cutaneous and mucocutaneous leishmaniasis

Tumour Necrosis Factor‐alpha (TNF‐α) and its soluble receptor type 1 (sTNFR I) in human active and healed leishmaniases

Effect of LACK and KMP11 on IFN‐γ Production by Peripheral Blood Mononuclear Cells from Cutaneous and Mucosal Leishmaniasis Patients

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