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. 2021 May:106:83-90.
doi: 10.1016/j.ijid.2021年02月01日6. Epub 2021 Feb 10.

Anti-Leishmania IgG is a marker of disseminated leishmaniasis caused by Leishmania braziliensis

Affiliations

Anti-Leishmania IgG is a marker of disseminated leishmaniasis caused by Leishmania braziliensis

Andréa Magalhães et al. Int J Infect Dis. 2021 May.

Abstract

Background: In this study, we determined the accuracy of anti-Leishmania IgG and IgG subclasses to distinguish clinical forms of American tegumentary leishmaniasis (ATL) and and determined the relationship between antibodies levels with cytokine production and severity of ATL.

Methods: Participants were 40 patients with cutaneous leishmaniasis (CL), 20 patients with mucosal leishmaniasis (ML), 20 patients with disseminated leishmaniasis (DL), and 20 individuals with subclinical Leishmania braziliensis infection (SC). Diagnosis was performed by DNA of L. braziliensis or IFN-γ production in SC. IgG and subclasses of IgG to soluble Leishmania antigen and cytokine levels in supernatants of mononuclear cells were detected by ELISA.

Results: IgG was detected in 95%, 95%, and 100% of patients with CL, ML, and DL, respectively. Higher levels of anti-Leishmania IgG and IgG2 were seen in DL compared to CL, ML, and SC. ROC analysis confirmed the ability of IgG to distinguish DL from the other clinical forms. A direct correlation was observed between IgG titers and levels of IFN-γ and CXCL10 in CL and DL, and IgG2 antibodies were correlated with the number of lesions in DL.

Conclusions: High anti-Leishmania IgG and IgG2 levels are characteristic of DL, and while IgG was correlated with pro-inflammatory cytokines, IgG2 was direct correlated with the number of lesions.

Keywords: Cutaneous leishmaniasis; Disease severity; Disseminated leishmaniasis; IgG; IgG2; Leishmania braziliensis.

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Conflict of interest statement

Potential conflicts of interest.

The authors declare no competing financial interests. All authors have submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest.

Figures

Figure 1.
Figure 1.. Clinical presentation of ATL caused by L. braziliensis.
A, 31-year-old male with CL presenting ulcerated lesion measuring ×ばつ26mm on the right leg at 30 days of illness. B and C, 65-year-old male patient with ML, previous history of cutaneous ulcer on the right leg for 8 months and nasal obstruction and mouth pain for 6 months. Large ulcer on the soft palate (B) and nasal septum perforation (C). D and E, 30-year-old male patient with DL presenting>100 mixed lesions (acneiform, crusted papules, superficial nodules and few ulcerations) on the face, trunk and limbs.
Figure 2.
Figure 2.. IgG anti-SLA in L. braziliensis clinical spectrum.
A, Total immunoglobulin (Ig) G response in L. braziliensis clinical spectrum (CL (n=40); ML (n=20); DL (n=20); and SC (n=20), 20 HS were used as controls. B, ROC curve analysis of IgG levels to distinguish DL patients from CL and ML subjects. C, detailed information obtained from each ROC curve is shown: Area Under Curve (AUC), P values of the ROC curves, the cut-off values chosen, and sensitivity and specificity with the 95% confidence interval (CI). Circles represent individual values; horizontal lines, median optical density (OD) values; dotted line in A, cutoff level. *P < .05, ***P < .0001.
Figure 3.
Figure 3.. IgG subclasses anti-SLA in L. braziliensis clinical spectrum.
IgG subclasses response in L. braziliensis clinical spectrum (CL (n=40); ML (n=20); DL (n=20); and SC (n=20), 20 HS were used as controls. A, IgG1. B, IgG2. C, IgG3. D, IgG4. Circles represent individual values; horizontal lines, median optical density (OD) values; dotted line, cutoff level. *P < .05; **P < .01, ***P < .0001.
Figure 4.
Figure 4.. ROC curve analysis of IgG2 levels to distinguish DL patients from CL and ML subjects.
A, ROC curves were built using IgG2 levels from L. braziliensis clinical spectrum (CL (n=40); ML (n=20); and DL (n=20). B, Detailed information obtained from each ROC curve is shown: Area Under Curve (AUC), P values of the ROC curves, the cut-off values chosen, and sensitivity and specificity with the 95% confidence interval (CI).
Figure 5.
Figure 5.. Correlation between humoral response and IFN-γ and CXCL-10 production in patients with cutaneous leishmaniasis and disseminated leishmaniasis.
A, Correlation between total immunoglobulin (Ig) G response and IFN-γ in CL patients (n = 24). B, correlation between IgG response and CXCL-10 IFN-γ in CL patients (n = 21). C, Correlation between anti-leishmania IgG antibodies and IFN-γ levels in DL (n = 14). D, Correlation between leishmania IgG antibodies and CXCL-10 levels in DL (n = 14). Spearman correlation was used in the analysis.
Figure 6.
Figure 6.. Correlation between humoral response and number of lesions in DL patients.
A, Correlation between total immunoglobulin (Ig) G response to SLA and number of lesions in DL patients. B, correlation between IgG2 response and number of lesions in DL patients. Spearman correlation was used in the analysis.

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