Cyclosporin A decreases lymphocyte migration to the heart allograft through suppression of their L-selectin expression
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Updated: Oct 26, 2026

An Immunological Model for Heterotopic Heart and Cardiac Muscle Cell Transplantation in Rats
Published on: May 8, 2020
M Maksymowicz1, B Lukomska, A Ziółkowska
1Department of Surgical Research & Transplantology, Medical Research Center, Polish Academy of Sciences, Warsaw, Poland.
Insights
Cyclosporin A (CsA) treatment reduces CD62L molecule expression on rat lymphocytes, impacting their migration to organ allografts. This finding offers insights into CsA
Area of Science:
- Immunology
- Pharmacology
- Transplantation Biology
Background:
- Cyclosporin A (CsA) is an immunosuppressant impacting lymphocyte distribution and traffic to allografts.
- CsA's complex mechanism involves inhibiting T-cell activation and suppressing specific gene expressions.
- Understanding CsA's effects on lymphocyte adhesion molecules is crucial for optimizing transplant outcomes.
Purpose of the Study:
- To investigate the effect of CsA on the expression of key adhesion molecules on rat thoracic duct lymphocytes.
- To determine if CsA alters the surface expression of CD11a, CD18, CD44, CD54, and CD62L.
Main Methods:
- Rats were treated with CsA for seven days.
- Thoracic duct lymphocytes were isolated from treated rats.
- Flow cytometry was used to analyze the expression of adhesion molecules CD11a, CD18, CD44, CD54, and CD62L.
Main Results:
- CsA administration significantly decreased the expression of CD62L on circulating lymphocytes.
- No significant changes were observed in the expression of CD11a, CD18, CD44, or CD54.
Conclusions:
- Reduced CD62L expression on lymphocytes due to CsA may impair their migration to allografts.
- This modulation of lymphocyte trafficking by CsA could influence their distribution within host lymphoid tissues.
- Targeting CD62L may offer a strategy to modulate CsA's effects in transplantation.
Abstract:
Cyclosporin A (CsA) changes the distribution of the circulating pool of lymphocytes and decreases their traffic to organ allograft. The mechanism of this process is complex and includes, among others, inhibition of induction of nuclear factor of activated T cells and suppression of GM CSF and E-selectin expression. We studied the expression adhesion molecules CD11a, CD18, CD44, CD54 and CD62L on the thoracic duct lymphocytes of rats treated with CsA. The 7-day administration of CsA evidently decreased the expression of CD62L but did not affect the other adhesion molecules. Lower concentration of CD62L molecules on the surface of circulating lymphocytes may influence their migration to allograft and distribution in host lymphoid tissues.