Splenic irradiation combined with tumor irradiation promotes T cell infiltration in the tumor microenvironment and helps in tumor control.
Animals
Cell Movement
/ immunology
Chemokines
/ metabolism
Disease Models, Animal
Interleukin-1beta
/ metabolism
Lymphocytes, Tumor-Infiltrating
/ cytology
Mice
Neoplasms
/ prevention & control
Receptors, CXCR3
/ metabolism
Spleen
/ radiation effects
T-Lymphocytes
/ cytology
Treatment Outcome
Tumor Microenvironment
/ immunology
CXCR3
IL-1β
Splenic irradiation
Tumor infiltrating leucocytes
Tumor microenvironment
Journal
Biochemical and biophysical research communications
ISSN: 1090-2104
Titre abrégé: Biochem Biophys Res Commun
Pays: United States
ID NLM: 0372516
Informations de publication
Date de publication:
26 02 2019
26 02 2019
Historique:
received:
01
01
2019
accepted:
15
01
2019
pubmed:
27
1
2019
medline:
30
11
2019
entrez:
26
1
2019
Statut:
ppublish
Résumé
Locally applied radiation to the tumor is reported to stimulate systemic immune response. During radiotherapy to the abdominal cancer, spleen often receives certain dose, though as an important immune organ, little is known about the impact of splenic irradiation (SI) on systemic immune and local tumor control. Through a mice model, we found that the combination of SI with tumor irradiation (TI) helped in local control. The analysis of the tumor infiltrating leucocytes demonstrated that SI plus TI brought more T cell aggregation in the tumor microenvironment (TME), which helped in tumor control. Increased T cell infiltration may be partly due to higher expression of T cell chemokine in the TME and more expression of CXCR3 on the T cells in the spleen after SI. SI produced more IL-1β in the spleen, IL-1β stimulated the expression of CXCR3 on the T cells, and enhanced their migration ability. Taken together, radiation to the spleen combined with TI helped in local control through promoting T cell infiltration, and may be a considerable means to enhance the immunomodulatory of radiotherapy.
Identifiants
pubmed: 30678810
pii: S0006-291X(19)30085-3
doi: 10.1016/j.bbrc.2019.01.071
pii:
doi:
Substances chimiques
Chemokines
0
Cxcr3 protein, mouse
0
IL1B protein, mouse
0
Interleukin-1beta
0
Receptors, CXCR3
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
156-162Informations de copyright
Copyright © 2019. Published by Elsevier Inc.