Changes in lymphoid tissue after treatment with a gonadotropin releasing hormone antagonist in the neonatal marmoset (Callithrix jacchus).

PROBLEM: The effect of neonatal treatment with a gonadotropin releasing hormone (GnRH) antagonist on the morphology and distribution of lymphocytes in lymphoid tissue of the infant marmoset was examined.

METHOD OF STUDY: From a screened panel of antihuman antibodies for specific immune cells, antibodies for the CD20 and CD3 antigens showed excellent reactivity with marmoset tissue. Five sets of marmoset twins were treated with either the GnRH antagonist or a vehicle from birth, and were euthanized at 7 to 9 (3 sets) or 16 to 20 weeks (2 sets) of age. The spleen, thymus, and inguinal lymph nodes from each animal were processed for immunocytochemistry, and the number of cells expressing the CD20 and CD3 antigens were quantified.

RESULTS

Control twins exhibited high plasma levels of testosterone, characteristic of the neonatal period, whereas testosterone concentrations were reduced (P = 0.001) to detection limits in the GnRH antagonist-treated twins. Microscopic evaluation suggested that treatment reduced the volume and cellularity of the thymic cortex, resulting in a decrease in the cortical-to-medullary ratio. Treatment reduced (P = 0.046) the number of thymocytes expressing the B-cell antigen (CD20) and marginally lowered (P = 0.067) the number expressing the T-cell antigen (CD3) in the thymic medulla. In the spleens of treated animals, periarterial lymphatic sheaths were less prominent on microscopic examination, and there were marginally fewer (P = 0.064) CD3+ cells. Numbers of CD20+ lymphocytes in the peripheral white pulp of the spleen and in the germinal centers of the lymph nodes, or CD3+ cells in the paracortex and germinal centers of the lymph nodes, were not altered by treatment.

CONCLUSION

Neonatal treatment with a GnRH antagonist may alter maturational processes for B and T cells in the thymus and spleen of the marmoset and may deprive the immune system of its normal sensitivity to GnRH at a potentially critical time in development.