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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

B-1 cells modulate the kinetics of wound-healing process in mice

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Author(s):
Oliveira, H. C. [1] ; Popi, A. F. [1, 2] ; Bachi, A. L. L. [1] ; Nonogaki, S. [3] ; Lopes, J. D. [1] ; Mariano, M. [1, 2]
Total Authors: 6
Affiliation:
[1] Univ Fed Sao Paulo, Discipline Immunol, Dept Microbiol Immunol & Parasitol, BR-04023900 Sao Paulo - Brazil
[2] Univ Paulista, Lab Biol Mol & Celular, Paulista - Brazil
[3] Hosp Canc, Fundacao Antonio Prudente, Sao Paulo - Brazil
Total Affiliations: 3
Document type: Journal article
Source: Immunobiology; v. 215, n. 3, p. 215-222, MAR 2010.
Web of Science Citations: 22
Abstract

Wound healing is a complex phenomenon whose mechanisms are not fully understood. Although inflammatory cells are recruited to the site of the lesion there are no reports concerning the participation of B lymphocytes in tissue repair. As demonstrated in our laboratory, B-1 cells migrate to a non-specific inflammatory focus and differentiate into a phagocyte. It has been reported that BALB/Xid mice are deficient in B-1 cells. Using this model, here we report that BALB/Xid mice have an increased inflammatory response, a delayed wound-healing process, a prominent neutrophilic infiltration of the lesion, and an increased neovascularization of the lesion as compared with BALB/c and BALB/Xid reconstituted with B-1 cells. The infiltration of B-1 cells into the wound was demonstrated. As B-1 cells secret and use interleukin 10 (IL-10) as an autocrine growth factor, the possible participation of this interleukin in the kinetics of wound healing was investigated. Results show that C57/BL6 IL-10 KO mice had an increased inflammatory response when compared with C57/BL6 and C57/BL6 IL-10 KO mice reconstituted with B-1 cells, thus suggesting that the observed effects of B-1 cells in the healing process is mediated by this interleukin. However, the mechanisms by which IL-10 influence these phenomena remain to be uncovered. (C) 2009 Elsevier GmbH. All rights reserved. (AU)

FAPESP's process: 04/08506-1 - B-1 cells: origin, differentiation and participation in inflammation, scarring and rejection of implant
Grantee:Mario Mariano
Support Opportunities: Research Projects - Thematic Grants