We thank the NIH/NCRR Resource MAPK Inhibitor Library for Nonhuman Primate Immune Reagents (Emory University, Atlanta, GA) for the macaque recombinant proteins; the NIH Division of Veterinary Resources (Bethesda, MD) for providing macaque blood samples; Dr Bernard A.P. Lafont (Laboratory of Molecular Microbiology, NIAID/NIH) for providing 721.221 cells; Drs Alison E. Hogg and L. Jean Patterson (Vaccine Branch, NCI/NIH) for helpful discussions; and Katherine M. McKinnon (Vaccine Branch Flow Cytometry Core, NCI/NIH) for expert advice. This research was supported by the Intramural Research Program of

the NIH, National Cancer Institute. Figure  S1. CD8α- macaque NK cells represent 35 percent of CD3-CD8α+ lymphocytes and express both CD56 and CD16. “
“Experimental autoimmune thyroiditis (EAT) is commonly induced by thyroglobulin (Tg) or Tg peptides in mice genetically susceptible to thyroiditis. In the present study, we investigated the immunogenic and pathogenic potential of a novel 20mer human Tg peptide, p2208 (amino acids 2208–2227), in mouse strains classified as low (LR) or high (HR) responders in EAT. The peptide was selected for its content in overlapping binding motifs for MHC class II products, associated with either resistance (Ab), or susceptibility

(As, Ek) to EAT. We therefore immunized LR BALB/c (H-2d) and C57BL/6 (H-2b) strains, as well as HR CBA/J (H-2k) Progesterone and SJL/J (H-2s) mice with 100 nmol of p2208 in adjuvant selleck chemicals and collected their sera, lymph nodes and thyroid glands for further analysis. The p2208 peptide was found to contain B-cell and cryptic T-cell epitope(s) in two of the

four strains examined, one LR and one HR. Specifically, it elicited direct EAT in C57BL/6 mice (two of seven mice, infiltration index 1–3), as well as in SJL/J mice (two of six mice, infiltration index 1–2). Such an EAT model could provide insights into the immunoregulatory cascades taking place in resistant hosts. “
“An oral delivery system based on ApxIIA#5-expressed on Saccharomyces cerevisiae was studied for its potential to induce immune responses in mice. Murine bone marrow-derived dendritic cells (DCs) stimulated in vitro with ApxIIA#5-expressed on S. cerevisiae upregulated the expression of maturation and activation markers, leading to production of tumor necrosis factor-α, interleukin (IL)-1β, IL-12p70 and IL-10. Presentation of these activated DCs to cluster of differentiation CD4+ T cells collected from mice that had been orally immunized with the ApxIIA#5-expressed on S. cerevisiae elicited specific T-cell proliferation.