Role of self carriers in the immune response and tolerance. III. B cell tolerance induced by hapten-modified-self involves both active T cell-mediated suppression and direct blockade

Scott, D.W.

Cellular Immunology 37(2): 327-335

1978


ISSN/ISBN: 0008-8749
PMID: 306890
DOI: 10.1016/0008-8749(78)90201-0
Accession: 068525819

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Abstract
The induction of B [bone marrow-derived] cell unresponsiveness with hapten-modified syngeneic murine lymphoid cells (hapten-modified self, HMS) can be achieved in vivo and in vitro. Tolerance in vivo in mice required a latent period of 3-4 days. B cell unresponsiveness could not be induced by HMS in athymic nude mice, although their nu/+ littermates were rendered hyporesponsive by HMS. Pretreatment of normal mice with cyclophosphamide (cyclo) prevented their susceptibility to tolerance induction by haptenated lymphoid cells. Nude mice became sensitive to HMS-induced suppression if they were first reconstituted with spleen cells from normal (but not cyclo-treated) donors. Labeling of H-2 antigens was not necessary for tolerance induction by HMS since haptenated teratoma [402AX] cells (lacking H-2) were tolerogenic in normal recipients. Suppression of the in vitro response to haptenated flagellin occurred equally well with nude, nu/+ and anti-Ly 2 + C-treated spleen cells. Cyclo-sensitive modified self-reactive (T [thymus-derived]) cells may regulate the immune response and mediate tolerance to HMS in vivo. The in vitro blockade of B cell reactivity may be directly mediated on hapten-specific PFC [plaque-forming cell] precursors.