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

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
Source :
Parasite Immunology. Nov2020, Vol. 42 Issue 11, p1-6. 6p.
Publication Year :
2020

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. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
01419838
Volume :
42
Issue :
11
Database :
Academic Search Index
Journal :
Parasite Immunology
Publication Type :
Academic Journal
Accession number :
146469408
Full Text :
https://doi.org/10.1111/pim.12772