Measles vaccination elicits T cell responses in infants as young as 6 months old, which may prime the humoral response to the second dose. Initiating measles vaccination as an early 2-dose regimen results in an immunologic response that is likely to have clinical benefits in developed and developing countries.

Vaccination of infants against measles remains of global importance, and proposed new vaccine strategies include the use of measles proteins or synthetic peptides as immunogens. We studied cell-mediated immunity to whole measles antigen and measles proteins in immune adults and infants after measles vaccine. Further, we measured CD8+ T cell responses to peptide pools corresponding to the nucelocapsid (N) measles protein in adults given measles vaccine. Cell-mediated immune responses to three of four measles proteins were equivalent to those against whole measles antigen in immune adults. Responses to the fusion (F) protein were lower in infants compared to whole measles antigen (p < or = 0.03). Infant responses to both whole measles antigen and the F protein were lower compared with these responses in adults (p < or = 0.001). CD8+ T cell responses to N peptide pools varied, and differed between immune HLA-A2-positive individuals compared with naive and HLA-A2-negative subjects after measles vaccination. The measles-specific T cell adaptive response of infants is limited compared to adults, including responses to the F protein.

SummaryThe BDC 2.5 T cell clone is specific for pancreatic ]3-cell antigen presented by I_Ag7, and greatly accelerates diabetes when injected into 10-21-d-old nonobese diabetic (NOD) mice. The BDC 2.5 T cell receptor (TCI<) has been solubilized as a TCR.-IgG1 chimeric protein.All NOD mice immunized against BDC 2.5 TCR-IgG1 produced antibodies recognizing TCP, C~x/C]3 epitopes that were inaccessible on the T cell surface. 56% of the mice produced antibodies against the BDC 2.5 clonotype that specifically blocked antigen activation of BDC 2.5 cells. We have used the adoptive transfer model of diabetes to demonstrate that maternal immunization with soluble TCR protects young mice from diabetes induced by the BDC 2.5 T cell clone.A s a result of the somatic recombination of TCR gene segments in developing T cells, each TCIL contains some structural epitopes that are unique to a particular T cell clone and some that are shared among different clones (1). Immunity against a TCR could therefore regulate the function of either a specific T cell clone or a set of clones in vivo, depending on the nature of the epitope recognized. In the rat and mouse models of experimental autoimmune encephalomyelitis (EAE) l, oligoclonal suppression of autoreactive T cells appeared to occur after immunization with peptides derived from the ix-or [3-chains of the TCIL of encephalitogenic T cells. Immunization of Lewis rats with synthetic peptides based on the V13-8.2 CDtL2 (2) or V~-D[3-JI3 (3) sequences of the TCP,. of rat encephalitogemc T cells suppressed the induction of EAE. immunization of B10.PL or (SJL × B10.PL) F i mice with a pepude derived from framework region 3 of the TCFL V[3-8.2 chain protected both strains against EAE (4, 5). Similar immunizations of DBA/2 or (PLJ × SJL) F 1 mice with a V[3-8.2 CDR2 peptide appeared to induce clonal anergy in all V[3-8.2 + T cells (6). The mechanism of regulation by TCIL 1Abbreviations used m thts paper, dc, dual chain; EAE, experimental autoammune encephalomyelitis; HRP, horseradish peroxtdase; MOI, multlphcity of refection; NOD, nonobese diabetic; sc, single chain; SS-, cell surface staining negative; SS +, cell surface staining poslnve. peptide immumzation is thought to involve primed CD4 + (5) or CD8 + (6) T cells that recognize the peptide in association with MHC molecules on the surface of either an APC or the autoreactive T cell itself (7). Although there are experimental data suggesting that T cells primed against the TCR V[3-8.2 CDR2 peptide can inhibit the activation of myelin basic protein--specific encephalitogenic rat T cells in vitro (8), the details and immunosuppressive effects of the mechanism are uncertain. T cells have yet to be shown to process their own TC1L and present MHC-associated epitopes. Likewise, it is not known whether professional APC present TCR epitopes derived from autoimmune T cells in the course of disease. Furthermore, in rat EAE, immunizatlon with the V~-8.2 CDIL2 peptide sometimes increased the seventy of disease and converted the normally acute, self...