Activated T cells induce expression of B7/BB1 on normal or leukemic B cells through a CD40-dependent signal.

摘要: Cognate interactions between antigen-presenting B and T cells play crucial roles in immunologic responses. that have been activated via the crosslinking of CD3 are able to induce cell proliferation immunoglobulin secretion a major histocompatibility complex-unrestricted contact-dependent manner. We find such human CD4+ cells, but not control Ig-treated may normal or leukemic express B7/BB1 significantly higher levels CD54 intercellular adhesion molecule 1 process also requires direct cell-cell contact. To discern what surface molecule(s) be responsible for signalling B7/BB1, we added various monoclonal antibodies (mAbs) specific accessory molecules mAbs cocultures alpha-CD3-activated resting cells. only alpha-CD40 can inhibit increased expression suggesting ligand CD40 expressed on an important inducer expression. Subsequent experiments fact demonstrate mAbs, changes phenotype similar those induced by when presented Fc gamma RII (CDw32)-expressing L These phenotypic significant effects function. Whereas chronic lymphocytic leukemia (CLL) normally very poor stimulators allogeneic mixed lymphocyte reactions (MLRs), CLL-B preactivated better presenters alloantigen, affecting up 30-fold-greater stimulation than treated nontreated Similarly, MLR stimulated nonleukemic enhanced if stimulator crosslinking. The generated inhibited blocking B7/BB1-CD28 interaction with CTLA4Ig. studies novel, CD40-dependent pathway inducing enhancing activity initiated contact alpha-CD3-stimulated