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Down-regulation of the CD62L antigen as a possible mechanism for neutrophilia during inflammation
O Rogowski1, Y Sasson, M Kassirer
1Department of Internal Medicine D, Tel-Aviv Sourasky Medical Centre, Israel.
Insights
Inflammation down-regulates CD62L (L-selectin) on white blood cells, correlating with increased neutrophils in circulation. This finding may explain neutrophil appearance during inflammatory conditions.
Area of Science:
- Immunology
- Hematology
Background:
- Leukocyte adhesion molecules play a critical role in inflammatory responses.
- CD62L (L-selectin) is involved in leukocyte rolling along the endothelium.
Purpose of the Study:
- To investigate the relationship between CD62L expression and white blood cell counts in patients with inflammatory conditions.
Main Methods:
- Quantified CD11b/CD18 and CD62L antigen expression on leukocytes.
- Determined absolute white blood cell counts in 116 patients.
- Analyzed correlations between cell counts and antigen expression.
Main Results:
- A significant negative correlation (P<0.0001, r=-0.57) was found between polymorphonuclear leukocyte count and CD62L expression.
- Down-regulation of CD62L was observed in patients with inflammatory conditions.
Conclusions:
- Reduced CD62L expression on neutrophils may contribute to their increased presence in peripheral blood during inflammation.
- This down-regulation could be a mechanism for leukocyte demargination in inflammatory states.
Abstract:
The expressions of both the CD11b/CD18 and CD62L (L-selectin) antigens as well as the absolute number of white blood cells in the peripheral circulating pool of blood in 116 patients with various inflammatory conditions were determined. A highly significant (P<0.0001) negative correlation (r = -0.57) was noted between the absolute number of peripheral blood polymorphonuclear leucocytes and the expression of the CD62L antigen on their surface. In view of the role of CD62L antigen in the rolling of leucocytes along endothelial cells in the microvasculature, its down-regulation might explain, at least in part, the demargination and appearance of neutrophilia during inflammation.