Figure 2From: Genetic variability in the rat Aplec C-type lectin gene cluster regulates lymphocyte trafficking and motor neuron survival after traumatic nerve root injury 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.Back to article page