Na. Lorr et al., DETECTION AND LOCALIZATION OF 3,3',4,4'-TETRACHLOROBIPHENYL-INDUCED P4501A PROTEIN IN AVIAN PRIMARY IMMUNE TISSUES, International journal of immunopharmacology, 16(10), 1994, pp. 875-885
P4501A can be detected in thymic and bursal microsomes from chickens p
retreated with 3,3',4,4'-tetrachlorobiphenyl (TCB) using a polyclonal
antibody against purified P4501A from 3-methylcholanthrene (3-MC)-indu
ced chicken embryo liver. A dose-response for induction by TCB of P450
1A protein was detected by Western blotting in both bursal and thymic
microsomes. Ethoxyresorufin-O-deethylase (EROD), a specific catalytic
activity of P4501A, was also induced in a dose-response fashion. More
TCB-induced P4501A was detected in thymus than bursa by both methods.
No EROD was detected in bursal or thymic microsomes from untreated chi
ckens, although P4501A protein was detected at very low levels in thym
ic microsomes from untreated chickens. P4501A was detected by immunohi
stochemistry in scattered patches of non-lymphocytic cells residing in
medullary regions of the TCB-induced thymus but was not detected in l
ymphocytes. This result supports previous work demonstrating that TCB-
inducible EROD is much higher in the supporting tissue cell fractions
than in lymphocyte fractions of the primary immune tissues. Although E
ROD was induced by TCB in the late stage embryo after 20 h exposure, n
o effect of TCB on the cell cycle in thymic or bursal lymphocytes was
observed over the same period. The same TCB exposure resulted in bursa
l but not thymic cellular depletion. Thymic and bursal supporting tiss
ue cells may be primary sites of immunosuppression within these organs
by P4501A inducers or substrates whether immunosuppression occurs sub
sequent to metabolism or through interaction with Ah receptors.