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12. |
- Raccosta, L, et al.
(författare)
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The oxysterol-CXCR2 axis plays a key role in the recruitment of tumor-promoting neutrophils
- 2013
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Ingår i: The Journal of experimental medicine. - : Rockefeller University Press. - 1540-9538 .- 0022-1007. ; 210:9, s. 1711-1728
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Tidskriftsartikel (refereegranskat)abstract
- Tumor-infiltrating immune cells can be conditioned by molecules released within the microenvironment to thwart antitumor immune responses, thereby facilitating tumor growth. Among immune cells, neutrophils play an important protumorigenic role by favoring neoangiogenesis and/or by suppressing antitumor immune responses. Tumor-derived oxysterols have recently been shown to favor tumor growth by inhibiting dendritic cell migration toward lymphoid organs. We report that tumor-derived oxysterols recruit protumor neutrophils in a liver X receptor (LXR)–independent, CXCR2-dependent manner, thus favoring tumor growth by promoting neoangiogenesis and immunosuppression. We demonstrate that interfering with the oxysterol–CXCR2 axis delays tumor growth and prolongs the overall survival of tumor-bearing mice. These results identify an unanticipated protumor function of the oxysterol–CXCR2 axis and a possible target for cancer therapy.
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- Sjöberg Wester, Elisabet, et al.
(författare)
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KEL*02 alleles with alterations in and around exon 8 in individuals with apparent KEL:1,-2 phenotypes.
- 2010
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Ingår i: Vox Sanguinis. - : Wiley. - 1423-0410 .- 0042-9007. ; May 4, s. 150-157
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Tidskriftsartikel (refereegranskat)abstract
- Background and Objectives Antibodies to antigens in the Kell blood group system, especially anti-KEL1, are involved in both haemolytic disease of the newborn and foetus and haemolytic transfusion reactions. Correct typing results are important and discrepancies between serologic and genetic typing must be resolved. Here, we describe the investigation of three healthy individuals who were initially phenotyped as KEL:1,-2. Materials and Methods Antigen typing was performed by standard serological techniques and by flow cytometric analysis. The KEL*01/02 polymorphism was tested by an allele-discrimination TaqMan assay as well as by PCR with allele-specific primers and PCR-RFLP. DNA sequencing of the KEL coding region was also performed. Results Two KEL*02N alleles with mutated splice sites around exon 8 were identified: intron 7 -1g>c (novel) and intron 8 +1g>t (previously reported in one case of K(0)). In the third sample, a missense mutation in exon 8, 787G>A (novel) predicting Gly263Arg, was detected on a KEL*02 allele and associated with dramatically weakened KEL2 antigen expression. Conclusion Resolution of discrepant phenotype/genotype results identified silencing mutations in or around exon 8. A combination of molecular and serologic methods has the potential to improve the quality of test results and was required to ensure both the accurate KEL2 antigen status and KEL*01 zygosity of these individuals.
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