Role of dendritic cells in the immune response induced by mouse mammary tumor virus superantigen

After mouse mammary tumor virus (MMTV) infection, B lymphocytes present a s uperantigen (Sag) and receive help from the unlimited number of CD4+ T cell s expressing Sag-specific T-cell receptor VP elements. The infected B cells divide and differentiate, similarly to what occurs in classical B-cell res ponses. The amplification of Sag-reactive T cells can be considered a prima ry immune response. Since B cells are usually not efficient in the activati on of naive T cells, we addressed the question of whether professional anti gen-presenting cells such as dendritic cells (DCs) are responsible for T-ce ll priming. We show here, using MMTV(SIM), a viral isolate which requires m ajor histocompatibility complex class II I-E expression to induce a strong Sag response in vivo, that transgenic mice expressing I-E exclusively on DC s (I-E alpha DC tg) reveal a strong Sag response. This Sag response was dep endent on the presence of Il cells, as indicated by the absence of stimulat ion in I-E alpha DC tg mice lacking B cells (I-E alpha DC tg mu MT-/-), eve n if these B cells lack I-E expression. Furthermore, the involvement of eit her residual transgene expression by B cells or transfer of I-E from DCs to B cells was excluded by the use of mixed bone marrow chimeras. Our results indicate that after priming by DCs in the context of I-E, the MMTV(SIM) Sa g can be recognized on the surface of B cells in the context of I-A. The mo st likely physiological relevance of the lowering of the antigen threshold required for T-cell/B-cell collaboration after DC priming is to allow B cel ls with a low affinity for antigen to receive T-cell help in a primary immu ne response.