B16 melanoma cells increase B-1 cell survival, IL-10 production and radioresistance in vitro

被引:10
作者
Lucatelli Laurindo, Maria Fernanda [1 ]
Thies, Felipe Garutti [1 ]
Perez, Elizabeth Cristina [1 ,2 ]
Novaes e Brito, Ronni Romulo [1 ]
Mariano, Mario [1 ,2 ]
Popi, Ana Flavia [1 ]
机构
[1] Univ Fed Sao Paulo, Dept Microbiol Immunol & Parasitol, Discipline Immunol, BR-04023900 Sao Paulo, Brazil
[2] Univ Paulista UNIP, Sao Paulo, Brazil
基金
巴西圣保罗研究基金会;
关键词
B-1; cells; B16; IL-10; Radioresistance; B-CELLS; MACROPHAGE POLARIZATION; MONONUCLEAR PHAGOCYTES; TRANSCRIPTION-3; STAT3; SIGNAL TRANSDUCER; DOWN-REGULATION; AUTOCRINE LOOP; IMMUNE CELLS; T-CELLS; INTERLEUKIN-10;
D O I
10.1016/j.imbio.2012.07.032
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
071005 [微生物学]; 100108 [医学免疫学];
摘要
B-1 cells can be differentiated from B-2 cells because they are predominantly located in the peritoneal and pleural cavities and have distinct phenotypic patterns and activation properties. The role of both cell populations in cancer progression is still controversial. Previous studies have indicated that direct contact between B-1 cells and B16 melanoma tumor cells (B16) increases the metastatic potential of the tumor cells. However, cellular changes that are induced in B-1 cells during the interaction between these two cell types have not been evaluated. In the present study, it is hypothesized that B-1 cells are modified after their interaction with tumor cells, leading to both increased cell viability and rate of proliferation. Additionally, soluble factors that were secreted by B16 cells were sufficient to augment B-1 cell viability and to modify the production of IL-10 by B-1 cells. Impressively, after direct or indirect contact with the B16 cells, B-1 cells became resistant to radiation-induced cell death. Thus, future studies that assess the importance of concomitant immunity and other conventional therapies in cancer treatment are needed. (C) 2012 Elsevier GmbH. All rights reserved.
引用
收藏
页码:609 / 619
页数:11
相关论文
共 46 条
[1]
Alas S, 2001, CANCER RES, V61, P5137
[2]
Mouse B-1 cell-derived mononuclear phagocyte, a novel cellular component of acute non-specific inflammatory exudate [J].
Almeida, SR ;
Aroeira, LS ;
Frymuller, E ;
Dias, MAA ;
Bogsan, CSB ;
Lopes, JD ;
Mariano, M .
INTERNATIONAL IMMUNOLOGY, 2001, 13 (09) :1193-1201
[3]
Inflammation and cancer: back to Virchow? [J].
Balkwill, F ;
Mantovani, A .
LANCET, 2001, 357 (9255) :539-545
[4]
Role of Stat3 in lipopolysaccharide-induced IL-10 gene expression [J].
Benkhart, EM ;
Siedlar, M ;
Wedel, A ;
Werner, T ;
Ziegler-Heitbrock, HWL .
JOURNAL OF IMMUNOLOGY, 2000, 165 (03) :1612-1617
[5]
A LINE OF NONTUMORIGENIC MOUSE MELANOCYTES, SYNGENEIC WITH THE B-16 MELANOMA AND REQUIRING A TUMOR PROMOTER FOR GROWTH [J].
BENNETT, DC ;
COOPER, PJ ;
HART, IR .
INTERNATIONAL JOURNAL OF CANCER, 1987, 39 (03) :414-418
[6]
BORRELLO MA, 1995, J IMMUNOL, V155, P4155
[7]
BORSELLINO N, 1995, CANCER RES, V55, P4633
[8]
De novo carcinogenesis promoted by chronic inflammation is B lymphocyte dependent [J].
de Visser, KE ;
Korets, LV ;
Coussens, LM .
CANCER CELL, 2005, 7 (05) :411-423
[9]
Global role of the immune system in identifying cancer initiation and limiting disease progression [J].
Disis, ML ;
Lyerly, HK .
JOURNAL OF CLINICAL ONCOLOGY, 2005, 23 (35) :8923-8925
[10]
FIORENTINO DF, 1991, J IMMUNOL, V146, P3444