| Abstract: | Inoculation of an immortalized clone of radiation leukemia virus (RadLV)-transformed antigen (ovalbumin, OVA)-specific T cells together with the relevant carrier (OVA) into unprimed syngeneic mice results in a preferential increase in the expression of anti-OVA antibodies of the immunoglobulin (Ig)G2b and IgG2a isotypes. Identical boosting of the clone-primed mice further augments the preferential production of anti-OVA antibodies of these two isotypes. The class-related helper activity is not due to nonspecific shift of class expression produced by the injected tumor cells, as a non-helper clone of RadLV-transformed T cells does not change the isotypic pattern of anti-OVA antibodies in the inoculated mice. A carrier-specific activation of the B cells is responsible for the class-restricted function of the helper clone. The isotypic profile of anti-hapten antibodies in mice injected with 2,4-dinitrophenyl (DNP)-bovine serum albumin and OVA-specific helper clone is not altered. On the other hand, mice inoculated with the OVA-specific helper clone and DNP-OVA respond with a preferential elevation of anti-DNP antibodies of the IgG2a and IgG2b isotypes. The preferential class augmentation may result from carrier-specific signals delivered by the helper clone which activate B cells in vivo toward certain CH expression. Alternatively, the observed class pattern may be induced by an isotype noncommited helper clone which triggers selected population of B lymphocytes of defined differentiation status toward secretion of a restricted array of isotypes. Regardless of the mechanism of the clone-dependent class expression, the isotypic profile in most of the experiments clearly demonstrates that an antigen-specific helper clone may be one of the elements which regulates the class of antibodies to be produced in vivo under normal physiologic conditions. |
