THE TESTICULAR ANTIVIRAL DEFENSE SYSTEM - LOCALIZATION, EXPRESSION, AND REGULATION OF 2'5'-OLIGOADENYLATE SYNTHETASE, DOUBLE-STRANDED RNA-ACTIVATED PROTEIN-KINASE, AND MX PROTEINS IN THE RAT SEMINIFEROUS TUBULE
N. Dejucq et al., THE TESTICULAR ANTIVIRAL DEFENSE SYSTEM - LOCALIZATION, EXPRESSION, AND REGULATION OF 2'5'-OLIGOADENYLATE SYNTHETASE, DOUBLE-STRANDED RNA-ACTIVATED PROTEIN-KINASE, AND MX PROTEINS IN THE RAT SEMINIFEROUS TUBULE, The Journal of cell biology, 139(4), 1997, pp. 865-873
Although the involvement of viruses in alterations of testicular funct
ion and in sexually transmitted diseases is well known, paradoxically,
the testicular antiviral defense system has virtually not been studie
d. The well known antiviral activity of interferons (IFNs) occurs via
the action of several IFN-induced proteins, among which the 2'5' oligo
adenylate synthetase (2'5' A synthetase), the double-stranded RNA-acti
vated protein kinase (PKR), and the Mx proteins are the best known. To
explore the antiviral capacity of the testis and to study the testicu
lar action of IFNs, we looked for the presence and regulation of these
three proteins in isolated seminiferous tubule cells, cultured in the
presence or in the absence of IFN alpha, IFN gamma, or Sendai virus.
In all conditions tested, the meiotic pachytene spermatocytes and the
post-meiotic early spermatids lacked 2'5' A synthetase, PKR, and Mx mR
NAs and proteins. In contrast, Sertoli cells constitutively expressed
these mRNAs and proteins, and their levels were greatly increased afte
r IFN alpha or Sendai virus exposure. While peritubular cells were als
o able to markedly express 2'5' A synthetase, PKR, and Mx mRNA and pro
teins after IFN alpha or viral exposure, only PKR was constitutively p
resent in these cells. Interestingly, IFN gamma had no effect on perit
ubular cells' 2'5' A synthetase and Mx production but it enhanced Mx p
roteins in Sertoli cells. In conclusion, this study reveals that the s
eminiferous tubules are particularly well equipped to react to a virus
attack. The fact that the two key tubular elements of the blood-testi
s barrier, namely, Sertoli and peritubular cells, were found to assume
this protection allows the extension of the concept of blood-testis b
arrier to the testicular antiviral defense.