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Related Concept Videos

T Cell Types and Functions01:24

T Cell Types and Functions

When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
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Updated: May 12, 2026

Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues
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Complement Anaphylatoxin C5a-Induced Mouse Lymphatic Functions Modulate Interactions Between Endothelial Cells and T

Haydn E Rich1, Yi-Dong Li2, Kathryn D Hok1

  • 1Center for Metabolic and Degenerative Diseases, Brown Foundation Institute of Molecular Medicine, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, TX 77030, USA.

Immune Network
|May 11, 2026
PubMed
Summary
This summary is machine-generated.

The complement factor C5a significantly impairs lymphatic function by reducing lymph propulsion and promoting Th1 cell polarization via the C5ar1-iNOS pathway. Targeting C5a/C5ar1 offers therapeutic potential for inflammatory diseases.

Keywords:
AnaphylatoxinsC5a receptor 1 signalingCD146-vimentin interactionCytokinesEndothelial functionEndothelial-T cell interactionLymphatic vesselsNitric oixide synthase type II

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Area of Science:

  • Immunology
  • Lymphatic System Biology
  • Vascular Biology

Background:

  • The lymphatic system is vital for immune cell trafficking.
  • Complement factors, particularly C5a, influence immune responses and vascular function.
  • Dysregulation of lymphatic function is implicated in chronic inflammatory diseases.

Purpose of the Study:

  • To investigate the impact of C5a and its receptor C5ar1 on lymphatic system function.
  • To elucidate the molecular mechanisms linking C5a signaling to lymphatic dysfunction and immune cell polarization.
  • To explore the therapeutic potential of targeting the C5a/C5ar1 axis in inflammatory conditions.

Main Methods:

  • Utilized wildtype and C5ar1-deficient C57B6/J mice models.
  • Administered acute C5a and lipopolysaccharide (LPS) challenges.
  • Assessed lymph propulsion dynamics.
  • Measured inducible nitric oxide synthase (iNOS) expression in endothelial cells.
  • Analyzed T helper cell polarization (Th1 subtypes).
  • Investigated protein interactions (CD146 and vimentin) on endothelial cells.

Main Results:

  • Acute C5a challenge significantly reduced lymph propulsion in wildtype mice compared to C5ar1-deficient mice.
  • C5ar1-dependent lymphatic dysfunction correlated with increased endothelial iNOS expression.
  • The C5a-iNOS axis promoted T helper cell polarization towards Th1 subtypes.
  • Observed C5a-mediated interaction between endothelial CD146 and Th1 cell vimentin, potentially facilitating cell transmigration.

Conclusions:

  • The C5a/C5ar1 axis plays a critical role in lymphatic dysfunction.
  • C5a signaling contributes to Th1 polarization and immune cell trafficking through endothelial iNOS.
  • Targeting C5ar1 presents a promising therapeutic strategy for managing chronic inflammatory diseases characterized by lymphatic dysfunction.