Necrosis, sarcolemmal damage and apoptotic events in myofibers rejected by CD8+ lymphocytes: Observations in nonhuman primates
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Updated: May 20, 2026

Immunolabelling Myofiber Degeneration in Muscle Biopsies
Published on: December 5, 2019
Daniel Skuk1, Jacques P Tremblay
1Neurosciences Division - Human Genetics, CHUQ Research Center - CHUL, Quebec, QC, Canada. Daniel.Skuk@fmed.ulaval.ca
Abstract:
To detect the mechanisms of death in allogeneic myofibers rejected by the immune system, myoblasts were allotransplanted in muscles of macaques immunosuppressed with tacrolimus. Immunosuppression was stopped 1month later to induce a massive rejection of allogeneic myofibers. Grafted sites were biopsied at 2-week intervals and analyzed by histology. The loss of allogeneic myofibers was rapid and concomitant with an intense infiltration of CD8+ lymphocytes. Several necrotic myofibers were observed in the lymphocyte accumulations by intracellular complement immunodetection. Dystrophin and spectrin immunodetection showed sarcolemmal damage in myofibers surrounded and invaded by CD8+ lymphocytes. Active caspase-3 was immunodetected in some myofibers surrounded by CD8+ lymphocytes. This is the first evidence that the collapse of myofibers attacked by T lymphocytes occurs by necrosis possibly due to damage of the sarcolemma. Caspase 3 is activated at least in some myofibers, but there was no evidence of a complete classical process of apoptosis.
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