Normal C57BL/10SnJ myoblasts were transplanted into the tibialis anter
ior of C57BL/10SnJ, C57BL/ScSn mdx; or BALB/c mice, These transplantat
ions allowed us to investigate the immunoresponse not only against MHC
but also against dystrophin introduced in the dystrophic muscles by s
uch transplantations. Recently, our group reported following myoblast
transplantations cellular infiltration of the host muscle by class II
MHC cells, macrophages, and lymphocytes expressing CD4 or CD8 and IL-2
receptors. In the present study, activation of these infiltrating lym
phocytes was investigated by measuring the expression of granzyme B mR
NA. We used reverse-transcriptase polymerase chain reaction to detect
granzyme B mRNA at various intervals after myoblast transplantations.
To standardize the results, the mRNA were reverse transcribed using an
oligo (dt) so that beta-actin mRNA could also be amplified from the s
ame cDNA preparation. Granzyme B mRNA was increased for at least 3 wee
ks after MHC alloincompatible grafts. The absence of increased granzym
e B expression after allocompatible transplantation in mdx mice sugges
ts that dystrophin is not sufficiently immunogenic to induce short ter
m acute rejection, These results indicate that lymphocytes infiltrated
in muscles injected with histoincompatible myoblasts are activated an
d sustain the requirement for an adequate immunosuppression after such
transplantations.