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Published on: July 28, 2010
CD23 and IgE expression during the human immune response to cutaneous leishmaniasis: possible role in monocyte
I Vouldoukis1, F Issaly, C Fourcade
1Laboratoire de Parasitologie Expérimentale, INSERM U313, Paris.
Insights
Serum IgE and TNF alpha levels correlate with CD23 expression in Leishmania brasiliensis infection. This immune response marker decreases after successful treatment but persists in therapy-resistant cases, suggesting a role for CD23 in cutaneous leishmaniasis.
Area of Science:
- Immunology
- Parasitology
- Dermatology
Background:
- Cutaneous leishmaniasis (CL) is caused by Leishmania brasiliensis.
- Immune responses involving T cells and macrophages are crucial in CL pathogenesis.
- Serum IgE and Fc epsilon RII/CD23 expression are implicated in inflammatory conditions.
Purpose of the Study:
- To analyze serum IgE levels and Fc epsilon RII/CD23 expression in L. brasiliensis-infected patients.
- To correlate these markers with inflammatory mediators like TNF alpha, IL-3, IFN gamma, and IL-4.
- To investigate the role of CD23 in the immune response to CL before and after therapy.
Main Methods:
- Serum IgE levels were measured in patients with CL.
- In situ expression of Fc epsilon RII/CD23, TNF alpha, IL-3, IFN gamma, and IL-4 mRNA was analyzed.
- Monocytes were purified to assess CD23 function in IgE/anti-IgE-dependent TNF alpha production.
- Comparisons were made between patients before and after treatment, and with disease-free individuals.
Main Results:
- Serum IgE and TNF alpha levels increased during L. brasiliensis infection.
- Elevated CD23, IL-4, and TNF alpha mRNA expression correlated with infection.
- These markers decreased after successful treatment but remained in therapy-resistant patients.
- Therapy-resistant patients showed reduced IFN gamma protein expression.
- CD23 mediates IgE/anti-IgE-dependent TNF alpha production in human monocytes.
Conclusions:
- Serum IgE and Fc epsilon RII/CD23 expression are associated with active Leishmania brasiliensis infection.
- CD23 plays a potential role in the acute immune response during human CL.
- Treatment outcomes in CL may be linked to the modulation of CD23 and IFN gamma expression.
Abstract:
Leishmania brasiliensis causes cutaneous leishmaniasis (CL) in humans. During this infection, a variety of inflammatory mediators are produced by T cells and monocytes/macrophages. In the present study, we analysed serum IgE levels and their correlation with in situ expression of the low affinity receptor for IgE (Fc epsilon RII/CD23) in patients infected with L. brasiliensis before and following therapy. These analyses were compared to in situ expression of tumour necrosis factor-alpha (TNF alpha), interleukin 3 (IL3), interferon-gamma (IFN gamma) and IL4. Disease-free individuals from the same endemic area sensitized with L. brasiliensis antigens were also included in this work. Our data indicate that during infection, serum levels of IgE and TNF alpha increased and correlated with elevated in situ expression of CD23, IL4 and TNF alpha mRNA. This expression disappeared following successful treatment, but persisted in patients resistant to anti-leishmania therapy. Patients resistant to therapy differed from other cases by a dramatic decrease in their in vivo expression of IFN gamma protein. Analysis of CD23 function in purified human monocytes indicated that this antigen mediates IgE/anti-IgE-dependent TNF alpha production. These data suggest a possible in vivo role of CD23 in acute immune responses in human CL.
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