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Updated: May 31, 2026

Blocking Lymph Flow by Suturing Afferent Lymphatic Vessels in Mice
05:59

Blocking Lymph Flow by Suturing Afferent Lymphatic Vessels in Mice

Published on: May 14, 2020

Cutting edge: JAM-C controls homeostatic chemokine secretion in lymph node fibroblastic reticular cells expressing

Vincent Frontera1, Marie-Laure Arcangeli, Claudia Zimmerli

  • 1INSERM, UMR891, Centre de Recherche en Cancérologie de Marseille, F-13009 Marseille, France.

Journal of Immunology (Baltimore, Md. : 1950)
|June 21, 2011
PubMed

Insights

This study identifies JAM-C as a key regulator of chemokine production in lymph nodes, crucial for maintaining these secondary lymphoid organs. Blocking JAM-C disrupts chemokine levels and affects T cell movement, highlighting its role in adult immune function.

Area of Science:

  • Immunology
  • Cell Biology
  • Developmental Biology

Background:

  • Secondary lymphoid organs like lymph nodes require coordinated development and maintenance.
  • Stromal cells produce lymphoid chemokines, but signals maintaining this production in adults are not fully understood.

Purpose of the Study:

  • To identify the specific cell populations and molecular mechanisms regulating chemokine production in adult lymph nodes.
  • To investigate the role of JAM-C in maintaining chemokine secretion and its impact on T cell egress.

Main Methods:

  • Utilized mice deficient in Jam-C and treated with anti-JAM-C antibodies.
  • Quantified intranodal content of key chemokines including CXCL12, CCL21, and CCL19.
  • Assessed naive T cell egress from lymph nodes.

Main Results:

  • Thrombomodulin and PDGF receptor α identified a specific fibroblastic reticular cell population.
  • JAM-C was found to control chemokine secretion in these cells.
  • Jam-C deficiency or blockade led to significant decreases in CXCL12, CCL21, and CCL19.
  • Reduced chemokine levels correlated with impaired naive T cell egress.

Conclusions:

  • JAM-C is essential for maintaining chemokine homeostasis in adult lymph nodes.
  • This pathway is critical for regulating T cell trafficking and immune surveillance.
  • Targeting JAM-C could influence immune cell migration and lymph node function.

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