CRIg signals induce anti‐intracellular bacterial phagosome activity in a chloride intracellular channel 3‐dependent manner

CRIg signals induce anti‐intracellular bacterial phagosome activity in a chloride intracellular channel 3‐dependent manner

Macrophages provide a first line of defense against bacterial infection by engulfing and killing invading bacteria, but intracellular bacteria such as Listeria monocytogenes (LM) can survive in macrophages by various mechanisms of evasion. Complement receptor of the immunoglobulin (CRIg), a C3b rece...

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Bibliographic Details
Published in:European journal of immunology Vol. 43; no. 3; pp. 667 - 678
Main Authors: Kim, Kwang H., Choi, Beom K., Song, Keoung M., Cha, Ki W., Kim, Young H., Lee, Ho, Han, In‐Seob, Kwon, Byoung S.
Format: Journal Article
Language:English
Published: Germany Wiley Subscription Services, Inc 01-03-2013
Subjects:
Animals
Bacteria
Bacterial infections
Cell Line
Chloride Channels - metabolism
Chlorides - metabolism
CLIC3
CRIg
Female
Humans
Listeria
Listeria monocytogenes - immunology
Lysosomes - immunology
Lysosomes - metabolism
Macrophages - immunology
Macrophages - metabolism
Macrophages - microbiology
Male
Membrane Fusion - immunology
Mice
Phagocytosis - genetics
Phagocytosis - immunology
Phagosome
Phagosomes - immunology
Protein Binding
Receptors, Complement - genetics
Receptors, Complement - metabolism
Receptors, Complement 3b - genetics
Receptors, Complement 3b - immunology
Receptors, Complement 3b - metabolism
Signal Transduction
Signaling
Vacuoles - immunology
Vacuoles - metabolism
Vacuoles - microbiology
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Summary:Macrophages provide a first line of defense against bacterial infection by engulfing and killing invading bacteria, but intracellular bacteria such as Listeria monocytogenes (LM) can survive in macrophages by various mechanisms of evasion. Complement receptor of the immunoglobulin (CRIg), a C3b receptor, binds to C3b on opsonized bacteria and facilitates clearance of the bacteria by promoting their uptake. We found that CRIg signaling induced by agonistic anti‐CRIg mAb enhanced the killing of intracellular LM by macrophages, and that this occurred in LM‐containing phagosomes. Chloride intra‐cellular channel 3 CLIC3, an intracellular chloride channel protein, was essential for CRIg‐mediated LM killing by directly interacting with the cytoplasmic domain of CRIg, and the two proteins colocalized on the membranes of LM‐containing vacuoles. CLIC3−/− mice were as susceptible to LM as CRIg−/− mice. These findings identify a mechanism embedded in the process by which macrophages take up opsonized bacteria that prevents the bacteria from evading cell‐mediated killing.
Bibliography:These authors contributed equally to this work.
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ISSN:0014-2980
1521-4141
DOI:10.1002/eji.201242997