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CD73-generated adenosine restricts lymphocyte migration into draining lymph nodes.

Masahide Takedachi¹, Dongfeng Qu, Yukihiko Ebisuno

¹Immunobiology and Cancer Program, Oklahoma Medical Research Foundation, 825 Northeast 13th Street, Oklahoma City, OK 73104, USA.

Journal of Immunology (Baltimore, Md. : 1950)

|April 22, 2008

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This summary is machine-generated.

CD73 (ecto-5'-nucleotidase) on high endothelial venules (HEV) controls lymphocyte migration into lymph nodes during inflammation. Its absence increases migration, highlighting adenosine receptor signaling

Area of Science:

Immunology
Cell Biology
Molecular Biology

Background:

Lymphocyte migration into lymph nodes is crucial for immune responses.
CD73 (ecto-5'-nucleotidase) produces adenosine and is present on high endothelial venules (HEV) and lymphocytes.
Inflammatory stimuli dramatically increase lymphocyte trafficking to lymph nodes.

Purpose of the Study:

To investigate the role of CD73 in regulating lymphocyte migration into draining lymph nodes post-inflammation.
To identify the specific cell type expressing CD73 that influences this migration.
To explore the involvement of adenosine receptors in CD73-mediated regulation.

Main Methods:

Comparison of lymphocyte migration in CD73 knockout (cd73(-/-)) mice versus wild-type mice after LPS administration.

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Assessment of lymphocyte migration rates in wild-type mice receiving lymphocytes from both cd73(+/+) and cd73(-/-) donors.

Utilizing an HEV-like cell line (KOP2.16) to study adenosine receptor expression and function.

Pharmacological intervention using an A(2B) receptor agonist (BAY 60-6583) to assess its effect on lymphocyte migration.

Main Results:

CD73 knockout mice exhibited significantly larger draining lymph nodes and increased L-selectin-dependent lymphocyte migration.
Lymphocyte migration rates were comparable between cd73(+/+) and cd73(-/-) lymphocytes when transferred into wild-type recipients, implicating HEV-expressed CD73.
The A(2B) adenosine receptor was identified as a likely target on HEV, upregulated by TNF-alpha.
Administration of an A(2B) receptor agonist normalized the increased lymphocyte migration observed in cd73(-/-) mice.

Conclusions:

CD73 expressed on high endothelial venules plays a critical role in limiting lymphocyte migration into inflamed lymph nodes.
Adenosine generated by CD73, acting via the A(2B) receptor, is a key regulator of lymphocyte trafficking during inflammation.
This signaling pathway represents an important mechanism for controlling the magnitude of inflammatory responses.