Obligatory role of B cells and adherent accessory cells in the transfer of a defect in morphine-mediated antinociception in C57BL/6J-bg/bg (beige-J) mice.

C57BL/6J-bg/bg (beige-J) mice have a blunted antinociceptive response to intracerebroventricularly (i.c.v.) injected morphine in the tail-flick test. Beige-J mice are also immunologically defective and exhibit the pathology of Chediak-Higashi syndrome (CHS). We transferred by i.v. injection 2 x 10(7) mononuclear spleen cells, devoid of PMNs, obtained from beige-J mice to normal C57BL/6J-bg/+ littermates that do not exhibit CHS or a blunted antinociceptive response to morphine. After 8 days, the normal littermates demonstrated significant (P less than 0.05) reduction in their analgesic responsiveness to morphine. This phenomenon was found to require B-cells and adherent cells in the adoptively transferred spleen cells. B-cells that had been purified by panning on anti-Ig-coated plates were sufficient to transfer the analgesic defect unless adherent cells were removed prior to immunocytoadherence. T-cells, in the presence or absence of adherent cells, failed to transfer the decreased sensitivity to morphine. These results demonstrate a novel neuroimmune interaction whereby B-lymphocytes and adherent cells, or a substance derived from them, are able to affect the antinociceptive action of morphine.