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Figure 2 | Journal of Neuroinflammation

Figure 2

From: Genetic variability in the rat Aplec C-type lectin gene cluster regulates lymphocyte trafficking and motor neuron survival after traumatic nerve root injury

Figure 2

Microarray studies of expression of the Aplec complex genes and Cd69 following VRA and the specific characterization of Cd69 expression in T cells. Microarray expressional profiling of spinal cords from naïve and operated DA and Aplec rats was performed. A detailed study of all genes in the Aplec segment was performed, as well as of Cd69, a C-type lectin commonly used as a marker of T-cell activation, as bioinformatical enrichment analysis had revealed differential regulation of Cd69 between the strains. Clecsf6/Dcir1, Clec4a2/Dcir2, Clec4a3/Dcir3 and Clec4a1/Dcir4 were upregulated following injury in both strains (A-D). Expression of Clec4a3/Dcir3 and Clec4a2/Dcir2 was higher in Aplec rats and Clecsf6/Dcir1 in DA rats following VRA (A-C). Clec4b2/Dcar1, Clec4d/Mcl and Clec4e/Mincle were not regulated by either injury or strain (E-G). Cd69, which is not a part of the Aplec complex, was upregulated only in Aplec rats following injury (H). To decide whether the differential upregulation of Cd69 was caused by inherent T-cell differences, or rather by an increased T-cell influx, characterization of Cd69 expression was performed in naïve and stimulated T cells from DA and Aplec rats. This revealed no significant strain differences in either naïve (I) or stimulated (J) T cells, suggesting the increased expression in the Aplec spinal cords is derived from an increased number of T cells. VRA: ventral root avulsion.

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