Host Immune Responses in the Control of Leishmania Infection and New Forms of Therapy for Tegumentary Leishmaniasis
Deadline for manuscript submissions: 31 December 2024 | Viewed by 190
Interests: the immunopathogenisis of leishmaniasis; influence of helminthiasis in immune response of chronic inflammatory diseases and autoimmune diseases; immunotherapy in infectious diseases
Interests: immunoregulation of neglected tropical diseases, in particular Chagas disease, leishmaniasis and rheumatic heart disease; biomarkers of disease progression and severity and new immunotherapeutic approaches
Special Issues, Collections and Topics in MDPI journals
Immunologic responses in the different clinical forms of leishmaniasis vary considerably depending the species of leishmania, genotypic differences intraspecies, and clinical forms of the diseases (including visceral, cutaneous, mucosal, disseminated leishmaniasis, and diffuse cutaneous leishmaniasis). Moreover, about 20% of healthy subjects who reside in endemic areas have evidence of leishmania infection, but do not develop any disease. These individuals are considered to have asymptomatic or subclinical (SC) infection. There is a gap in the understanding of how some subjects control leishmanial infection, while in others the parasites proliferate and consequently develop disease. Additionally, it is not clear why parasites are easily detectable infections caused by some leishmania species such as Leishmania Viannia guyanensis and are scarce in diseases caused by L. braziliensis, as well as why parasites persist in macrophages despite the presence of the Th1 immune response. In American tegumentary leishmaniasis caused by L. braziliensis infection, macrophages produce reactive oxygen species and nitric oxide but have a limited ability to kill leishmania. In contrast, macrophages from subjects with SC infection are less permissive to leishmania penetration and kill parasites, even in the absence of a Th1 immune response. In subjects cured of CL, the ability to control leishmanial infection is restored and, despite the observation of a poor immune response in peripheral blood, there is a strong DTH to leishmania antigens. In mice, resident memory T cells, together with macrophages, control a new infection, but this subject has not been studied in humans.
Treatment failure in tegumentary leishmaniasis is on the rise and chemotherapy associated with immunostimulants or drugs that down-modulate inflammatory responses can enhance the cure rate and decrease the healing time of ulcers.
The focus of this Special Issue is to show how the immune response controls or facilitates parasite multiplication in human cells and the use of immunotherapy and chemotherapy in the treatment of tegumentary leishmaniasis.
Prof. Dr. Edgar Carvalho
Prof. Dr. Walderez Ornelas Dutra
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- leishmania killing
- dermal memory T cells
- subclinical leishmania infection
- cutaneous leishmaniasis
The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.
Title: Senescent CD8+T cells in the pathogenesis of disseminated leishmaniasis
Highlights: Disseminated Leishmaniasis; CD8+T cells; senescent.