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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 promote immunosurveillance against murine melanoma in host absence of CCR5: New perspective in autologous vaccination therapy

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Author(s):
Vivanco, Bruno C. [1] ; Viana, Jacqueline D. [1] ; Perez, Elisabeth C. [2] ; Konno, Fabiana T. C. [2] ; Guereschi, Marcia G. [1] ; Xander, Patricia [3] ; Keller, Alexandre C. [1, 4] ; Lopes, Jose D. [3, 1]
Total Authors: 8
Affiliation:
[1] Univ Fed Sao Paulo, Dept Microbiol Imunol & Parasitol, Sao Paulo - Brazil
[2] Univ Paulista, Sao Paulo - Brazil
[3] Univ Fed Sao Paulo, Dept Ciencias Biol, Sao Paulo - Brazil
[4] Univ Fed Sao Paulo, Dept Med, Sao Paulo - Brazil
Total Affiliations: 4
Document type: Journal article
Source: Immunobiology; v. 219, n. 11, p. 845-849, NOV 2014.
Web of Science Citations: 2
Abstract

Autologous vaccination with tumor-primed dendritic cells increases immune response against tumor, which seems to be improved in host absence of CCR5. Because B-1 lymphocytes modulate the activity of different immune cells, we decided to study their influence in the resistance against murine B16F10 melanoma in a CCR5 deprived environment. Adoptive transfer of peritoneal B-1 CCR5(+/+) lymphocytes to CCR5(-/-) animals inhibited the establishment of lung metastasis and melanoma cell growth, in comparison to saline-treated CCR5-/- mice. In loco cell analysis demonstrated that the adoptive transfer of B-1 CCR5(+/+) + lymphocytes to CCR5 deficient host was associated with a more intense influx of T CD8(+) to tumor site, indicating that the presence of CCR5(+/+) B-1 cells in the tumor environment induces the migration of T CD8 CCR5(-/-) cells to the implantation site. To corroborate this idea, CCR5(-/-) mice were injected with non B-1 peritoneal cells from wild type (WT) mice before B16F10 inoculation. In this regimen, CCR5(-/-) mice were not protected from tumor growth reinforcing the idea that, in host absence of CCR5, B-1 cells are essential to confer tumor resistance. This work indicates that, in the host absence of CCR5, naive B-1 cells may activate CD8T lymphocytes thereby promoting tumor resistance. Our results strongly suggest that autologous vaccination with B-1 lymphocytes in combination with CCR5 antagonists can be an alternative approach to tumor therapy. (C) 2014 Elsevier GmbH. All rights reserved. (AU)

FAPESP's process: 11/50256-6 - B-1 cells: biology, relations with other cells of the immune system and participation in different experimental models
Grantee:José Daniel Lopes
Support Opportunities: Research Projects - Thematic Grants