Journal
SCIENCE
Volume 314, Issue 5798, Pages 454-458Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1133515
Keywords
-
Categories
Funding
- Medical Research Council [G108/485, G9800943] Funding Source: researchfish
- MRC [G9800943, G108/485] Funding Source: UKRI
- Medical Research Council [G9800943, G0600823, G108/485] Funding Source: Medline
- Wellcome Trust [077273] Funding Source: Medline
Ask authors/readers for more resources
An effective host immune response to mycobacterial infection must control pathogen dissemination without inducing immunopathology. Constitutive overexpression of mycobacterial heat shock protein (myHsp70) is associated with impaired bacterial persistence, but the immune-mediated mechanisms are unknown. We found that myHsp70, in addition to enhancing antigen delivery to human dendritic cells, signaled through the CCR5 chemokine receptor, promoting dendritic cell aggregation, immune synapse formation between dendritic cells and T cells, and the generation of effector immune responses. Thus, CCR5 acts as a pattern-recognition receptor for myHsp70, which may have implications for both the pathophysiology of tuberculosis and the use of myHsps in tumor-directed immunotherapy.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available