We have produced a panel of islet-specific T-cell clones from nonobese diabetic (NOD) mice. These clones proliferate and make interleukin 2 in an antigen-specific manner in response to NOD antigen-presenting cells and islet cells. Most of the clones respond to islet-cell antigen from different mouse strains but only in the presence of antigen-presenting cells bearing the class II major histocompatibility complex of the NOD mouse. In vivo, the clones mediate the destruction of islet, but not pituitary, grafts. Furthermore, pancreatic sections from a disease transfer experiment with one of the clones showed a pronounced cellular infiltration and degranulation of islets in nondiabetic (CBA x NOD)F1 recipients.
A cloned T-lymphocyte line, BDC-2.5, was derived from a nonobese diabetic (NOD) mouse and has been found to exhibit specificity for islet cell antigen in vitro and in vivo. This clone is a CD4+ T-lymphocyte that proliferates and makes lymphokine in response to islet cell antigen- and NOD antigen-presenting cells. In an in vivo transplantation system in which islet grafts were made in the presence or absence of the BDC-2.5 T-lymphocytes, it was found that incorporation of the islet-specific T-lymphocytes into the graft site resulted in complete destruction of the transplanted tissue. Similar grafts made with pituitary tissue were not affected by the T-lymphocyte clone. These results suggest that the islet-specific T-lymphocytes mediate islet destruction in a tissue-specific manner.
Objective. The shared epitope hypothesis posits that amino acids QR/KRAA in positions 70-74 of the DRB1 chain are responsible for rheumatoid arthritis susceptibility. However, even DRB1*04 alleles containing the shared epitope vary greatly with respect to degrees of susceptibility. This study was undertaken to conduct a molecular examination of the shared epitope hypothesis by measuring binding of arthritogenic peptides to susceptibility and resistance alleles.Methods. We measured binding of native and citrullinated forms of vimentin 66-78 and a-enolase [11][12][13][14][15][16][17][18][19][20][21][22][23][24][25] and noncitrullinated type II collagen [258][259][260][261][262][263][264][265][266][267][268][269][270][271][272] to 88 class II alleles on Luminex beads (which includes alleles of many varying degrees of susceptibility and resistance).
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