Th17 lymphocytes in atypical cutaneous leishmaniasis caused by Leishmania (L.) infantum chagasi in Central America. (15th July 2020)

• Record Type: Journal Article
• Authors: Araujo Flores, Gabriela Venicia; Sandoval Pacheco, Carmen Maria; Sosa Ochoa, Wilfredo Humberto; Gomes, Cláudia Maria Castro; Zúniga, Concepción; Corbett, Carlos P.; Laurenti, Marcia Dalastra
• Is Part Of: Parasite immunology. Volume 42:Number 11(2020)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2020-07-15
• Subjects: cellular immune response -- Leishmania infantum chagasi -- leishmaniasis -- Th17 cells; Veterinary parasitology -- Immunological aspects -- Periodicals; Host-parasite relationships -- Immunological aspects -- Periodicals; 571.96
• DOI: 10.1111/pim.12772
• Languages: English
• ISSNs: 0141-9838

Abstract

Abstract: Skin lesions in nonulcerated cutaneous leishmaniasis (NUCL) caused by Leishmania (L.) infantum chagasi are characterized by a mononuclear inflammatory infiltrate in the dermis, which is composed mainly of lymphocytes, followed by macrophages, few plasma cells and epithelioid granulomas with mild tissue parasitism. Previous studies have shown that the main population of lymphocytes present in the dermal infiltrate is CD8 + T cells, followed by CD4 + T cells, which are correlated with IFN‐γ + cells. To improve the knowledge of cellular immune responses in NUCL, skin biopsies were submitted to immunohistochemistry using anti‐ROR‐γt, anti‐IL‐17, anti‐IL‐6, anti‐TGF‐β, and anti‐IL‐23 antibodies to characterize the involvement of Th17 cells in the skin lesions of patients affected by NUCL. ROR‐γt +, IL‐17 +, IL‐6 +, TGF‐β + and IL‐23 + cells were observed in the dermal inflammatory infiltrate of NUCL skin lesions. A positive correlation between CD4 + T‐lymphocytes and ROR‐γt + and IL‐17 + cells suggests that some of the CD4 + T‐lymphocytes in NUCL could be Th17 lymphocytes. Moreover, a positive correlation between ROR‐γt + cells and TGF‐β +, IL‐6 +, IL‐17 + and IL‐23 + cells could indicate the role of these cytokines in the differentiation and maintenance of Th17 lymphocytes. Our findings improve knowledge of the pathogenesis of this rare and atypical clinical form of leishmaniasis.