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Effects of extracellular vesicles released by peritoneal B‐1 cells on experimental Leishmania ( Leishmania ) amazonensis infection
Author(s) -
Toledo Maytê dos Santos,
CronembergerAndrade André,
Barbosa Fernanda Marins Costa,
Reis Natasha Ferraz de Campos,
Dupin Talita Vieira,
Soares Rodrigo Pedro,
Torrecilhas Ana Claudia,
Xander Patricia
Publication year - 2020
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.3ma0220-464rr
Subject(s) - biology , immune system , leishmania , immunology , leishmania major , bone marrow , immunity , microbiology and biotechnology , parasite hosting , world wide web , computer science
B‐1 cells are a B‐lymphocyte subtype whose roles in immunity are not completely defined. These cells can produce cytokines (mainly IL‐10) and natural and specific antibodies. Currently, extracellular vesicles (EVs) released by immune cells have emerged as new important entities in cell‐cell communication. Immune cells release EVs that can activate and/or modulate other immune cells. Here, we characterized the EVs released by peritoneal B‐1 cells infected or not with Leishmania ( Leishmania ) amazonensis . This Leishmania species causes cutaneous leishmaniasis and can infect macrophages and B‐1 cells. Our results showed that peritoneal B‐1 cells spontaneously release EVs, but the parasite stimulated an increase in EVs production by peritoneal B‐1 cells. The treatment of BALB/c and C57BL/6 bone marrow‐derived macrophages (BMDM) with EVs from infected peritoneal B‐1 cells led to differential expression of iNOS, IL‐6, IL‐10, and TNF‐α. Additionally, BALB/c mice previous treated with EVs released by peritoneal B‐1 cells showed a significant lower lesion size and parasite burden. Thus, this study demonstrated that peritoneal B‐1 cells could release EVs that can alter the functions of macrophages in vitro and in vivo these EVs altered the course of L. amazonensis infection. These findings represent the first evidence that EVs from peritoneal B‐1 cells can act as a new mechanism of cellular communication between macrophages and B‐1 cells, contributing to immunity against experimental leishmaniasis.