| Full text | |
| Author(s): |
Perez, Elizabeth Cristina
[1, 2]
;
Xander, Patricia
[3]
;
Lucatelli Laurindo, Maria Fernanda
[1]
;
Novaes e Brito, Ronni Romulo
[4]
;
Vivanco, Bruno Camolese
[1]
;
Mortara, Renato Arruda
[1]
;
Mariano, Mario
[1, 2]
;
Lopes, Jose Daniel
[1]
;
Keller, Alexandre Castro
[1, 5]
Total Authors: 9
|
| Affiliation: | [1] Univ Fed Sao Paulo Escola Paulista Med UNIFESP EPM, Dept Microbiol Immunol & Parasitol, Sao Paulo, SP - Brazil
[2] Univ Paulista, Environm & Expt Pathol Program, Sao Paulo, SP - Brazil
[3] Univ Fed Sao Paulo, Dept Pharmaceut Sci, Campus Diadema, Diadema, SP - Brazil
[4] Ctr Univ Sao Camilo, Sao Paulo, SP - Brazil
[5] Univ Fed Sao Paulo Escola Paulista Med UNIFESP EPM, Nephrol Div, Dept Med, Sao Paulo, SP - Brazil
Total Affiliations: 5
|
| Document type: | Journal article |
| Source: | PLoS One; v. 12, n. 11 NOV 16 2017. |
| Web of Science Citations: | 0 |
| Abstract | |
B-1 lymphocytes are known to increase the metastatic potential of B16F10 melanoma cells via the extracellular signal-regulated kinase (ERK) pathway. Since IL-10 is associated with B-1 cells performance, we hypothesized that IL-10 could be implicated in the progression of melanoma. In the present work, we found that the C57BL/6 mice, inoculated with B16F10 cells that were co-cultivated with B-1 lymphocytes from IL-10 knockout mice, developed fewer metastatic nodules than the ones which were injected with the melanoma cells that were cultivated in the presence of wild-type B-1 cells. The impairment of metastatic potential of the B16F10 cells was correlated with low activation of the ERK signaling pathway, supporting the idea that the production of IL-10 by B-1 cells influences the behavior of the tumor. A microarray analysis of the B-1 lymphocytes revealed that IL-10 deficiency is associated with down-regulation of the genes that code for claudin-10, a protein that is involved in cell-to-cell contact and that has been linked to lung adenocarcinoma. In order to determine the impact of claudin-10 in the cross-talk between B-1 lymphocytes and the B16F10 tumor cells, we took advantage of small interfering RNA. The silencing of claudin-10 gene in B-1 lymphocytes inhibited activation of the ERK pathway and abrogated the B-1-induced aggressive behavior of the B16F10 cells. Thus, our findings suggest that the axis IL-10/claudin-10 is a promising target for the development of therapeutic agents against aggressive melanoma. (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 |
| FAPESP's process: | 08/50632-5 - Identificacao e caracterizacao de molecula expressa nos linfocitos b-1 que induz aumento o potencial metastatico de celulas de melanoma murino b16. |
| Grantee: | ELIZABETH CRISTINA PEREZ HURTADO |
| Support Opportunities: | Scholarships in Brazil - Post-Doctoral |
| FAPESP's process: | 16/02189-1 - Incorporation of glycosphingolipids into nanoparticles to immunotherapy using invariant Natural Killer T lymphocytes |
| Grantee: | Alexandre de Castro Keller |
| Support Opportunities: | Regular Research Grants |