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Published on: May 31, 2018
Tetraspanin CD82 restrains phagocyte migration but supports macrophage activation
Erin N S McGowan1, Osanna Wong2, Eleanor Jones2,3
1Department of Biochemistry and Pharmacology, Bio21 Molecular Science and Biotechnology Institute, The University of Melbourne, Parkville, VIC 3052, Australia.
Abstract:
Phagocytes migrate into tissues to combat infection and maintain tissue homeostasis. As dysregulated phagocyte migration and function can lead to inflammation or susceptibility to infection, identifying molecules that control these processes is critical. Here, we show that the tetraspanin CD82 restrains the migration of neutrophils and macrophages into tissues. Cd82 phagocytes exhibited excessive migration during in vivo models of peritoneal inflammation, superfusion of CXCL1, retinopathy of prematurity, and infection with the protozoan parasite L. mexicana. However, with the latter, while Cd82 macrophages infiltrated infection sites at higher proportions, cutaneous L. mexicana lesions were larger and persisted, indicating a failure to control infection. Analyses of in vitro bone-marrow-derived macrophages showed CD82 deficiency altered cellular morphology, and impaired gene expression and metabolism in response to anti-inflammatory activation. Altogether, this work reveals an important role for CD82 in restraining phagocyte infiltration and mediating their differentiation in response to stimulatory cues.
Insights
The tetraspanin CD82 limits immune cell (phagocyte) migration into tissues. CD82 deficiency leads to excessive phagocyte infiltration but impairs infection control, highlighting CD82
Area of Science:
- Immunology
- Cell Biology
- Molecular Biology
Background:
- Phagocyte migration is crucial for combating infection and maintaining tissue health.
- Dysregulated phagocyte function can result in inflammation or increased infection susceptibility.
- Identifying regulatory molecules controlling phagocyte migration is critical.
Purpose of the Study:
- To investigate the role of the tetraspanin CD82 in regulating phagocyte migration and function.
- To determine how CD82 deficiency impacts immune responses in various inflammatory and infectious models.
Main Methods:
- In vivo studies using mouse models of peritoneal inflammation, CXCL1 superfusion, retinopathy of prematurity, and Leishmania mexicana infection.
- In vitro analysis of bone-marrow-derived macrophages.
- Assessment of phagocyte migration, lesion development, cellular morphology, gene expression, and metabolism.
Main Results:
- Phagocytes lacking CD82 (Cd82-/-) showed excessive migration into tissues across multiple models.
- Despite increased infiltration, Cd82-/- macrophages failed to control Leishmania mexicana infection, leading to larger, persistent lesions.
- CD82 deficiency altered macrophage morphology and impaired their gene expression and metabolism during anti-inflammatory activation.
Conclusions:
- CD82 acts as a crucial restraint on neutrophil and macrophage migration into tissues.
- CD82 is essential for effective phagocyte function, including controlling parasitic infections and mediating appropriate responses to inflammatory cues.
- This study reveals a significant role for CD82 in regulating both phagocyte infiltration and differentiation.
