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Hui Shao

Publications and source records attributed to Hui Shao.

25 records · Page 2Linked to original sources
PubMed2003

Infiltration of the inflamed eye by NKT cells in a rat model of experimental autoimmune uveitis.

NK and NKT cells play important roles in both the pathogenesis and regulation of autoimmune disease. In this study, NK and NKT cells in the periphery and in the inflamed eyes of Lewis rats developing uveitis were quantified and evaluated for function. The number and phenotype of NK/NKT cells in the inflamed eyes and spleens were determined. The cytotoxic and suppressive activity of the eye-infiltrating NK/NKT cells was also studied. In rats with interphotoreceptor retinoid-binding protein (IRBP)-induced uveitis, the number of NK/NKT cells declined in the periphery, but increased in the eyes. The eye-infiltrating NK/NKT cells inhibited cytokine production by autoreactive T cells in vitro and had a weak cytolytic effect on NK-sensitive YAC-1 cells and NKT-sensitive U937 cells in vitro. Our study shows that the number of NK and NKT cells decreases in the periphery of rats with autoimmune uveitis. It is discussed whether the changing number of NK/NKT cells allows the escape from immune surveillance of uveitogenic (i.e. autoreactive) T cells and the development of intraocular inflammation, and the increased infiltration of the inflamed eye by suppressive NK/NKT cells favors rapid recovery from disease.

Animals↗
PubMed2003

Encephalitogenic activity of truncated myelin oligodendrocyte glycoprotein (MOG) peptides and their recognition by CD8+ MOG-specific T cells on oligomeric MHC class I molecules.

We have previously demonstrated that the 21-residue peptide pMOG(35-55) from myelin oligodendrocyte glycoprotein (MOG) contains an antigenic epitope that activates CD8(+) encephalitogenic T cells in C57BL/6 (B6) mice. To identify the core encephalitogenic epitope of CD8(+) MOG-specific T cells, we have prepared a panel of highly purified peptides of varying lengths, which span the entire length of pMOG(35-55), and tested their binding to recombinant H-2D(b) dimers and their ability to induce EAE. Two of the truncated peptides, pMOG(40-54) and pMOG(44-54), strongly bound recombinant H-2D(b) protein and this complex bound MOG-specific CD8(+) T cells. Interestingly, pMOG(40-54) retained the full capability of inducing paralytic disease, whereas only a part of the B6 mice immunized with pMOG(44-54) developed clinical paralysis and central nervous system (CNS) inflammation. Further deletion of 1 amino acid from either the N- or C-terminus of the peptide pMOG(44-54) dramatically reduced binding to recombinant H-2D(b), and abolished the induction of paralysis and CNS inflammation. Our results demonstrate that the ability of truncated pMOG(35-55) peptides to bind recombinant H-2D(b) protein does not always correlate with their ability of inducing encephalomyelitis. This approach enables the further identification of the core pathogenic epitope within the pMOG(35-55) that activates MOG-specific encephalitogenic CD8(+) T cells.

Animals↗
PubMed2003

A sequence function reveals new features in beta-protein folding.

When amino acid residues are represented by parameters describing their side chain lengths and polarities, a sequence function defined as the sum of the first two sequence autocorrelation functions is found to be negatively and linearly correlated with the logarithms of folding rates of beta-proteins. The new function reveals new features in beta-protein folding: larger residues slow down the folding while alternative distribution of polar-non-polar residues accelerates the folding.

Amino Acid Sequence↗
PubMed2003

A simple parameter relating sequences with folding rates of small alpha helical proteins.

It is found that the helix parameter (HP), which favors clustering of non-polar residues, is linearly correlated with the logarithms of rate constants of folding of small two-state alpha-helical proteins. The definition is HP = N(H)(-1) sigma [f(i)+ (f(i-1)+f(i+1))/2], where f(i)=1 or -1, if the i'th residue is hydrophobic or hydrophilic, respectively, N(H) is the number of hydrophobic residues and the summation is taken over the hydrophobic residues.

Algorithms↗
PubMed2002

Induction of autoimmune encephalomyelitis and uveitis in B6 and (B6 x SJL) mice by peptides derived from myelin/oligodendrocyte glycoprotein.

Previous studies have shown that immunization of the Lewis rat with myelin basic protein (MBP), an encephalitogenic antigen derived from the myelin sheath of the CNS, induced both experimental autoimmune encephalomyelitis (EAE) and anterior uveitis (AU). In the current study, we show that a major peptide derived from another encephalitogenic myelin protein-the myelin/oligodendrocyte glycoprotein (MOG35-55)-induced both encephalomyelitis and uveitis in (B6 x SJL) F1 and wt-B6 mice. Pathological studies documented that an anterior uveitis was induced by MOG35-55. A similar disease pattern was induced by either active immunization with peptideMOG35-55 (pMOG35-55) or adoptive transfer of MOG35-55-specific T cells. The induced uveitis persisted for >60 days without remission. Our studies demonstrate for the first time that MOG is uveitogenic in mice that express the H-2(b) genetic background. This new experimental model should provide a useful tool for the study of the pathogenesis of chronic AU and determination of the pathogenic mechanisms by which a large portion of MS patients develops uveitis.

Adoptive Transfer↗
PubMed2002

Expression of B7 molecules in the eye during experimental autoimmune anterior uveitis (EAAU).

PURPOSE: We have reported that CTLA4-Fc, a fusion protein that binds B7, prevents the induction of EAAU and reduces the severity of disease in Lewis rats. Since B7.1 and B7.2 have distinctive roles in other autoimmune diseases, we investigated their roles in the development of EAAU. METHODS: Lewis rats were immunized with melanin associated antigen (MAA). Eyes were collected at different stages of EAAU and the expression of B7 on iris and ciliary body (ICB) cell suspensions determined by flow cytometry analysis. The incidence of EAAU after treatment with anti B7, and the requirement of B7.1 and B7.2 for proliferation and cytokine production of lymphoid cells to MAA were also studied. RESULTS: B7.2 is up-regulated in resident ICB cells or bone-marrow derived cells which have infiltrated the ICB by day 10 and remains elevated during the acute phase of disease. B7.1 is expressed later during the acute phase. Both B7.1 and B7.2 are down-regulated during remission, with low levels of B7.2 and no detectable B7.1. The incidence of EAAU was reduced by anti-B7.2 treatment and completely inhibited by a combination of both B7.1 and B7.2 antibodies. Neither anti-B7.1 nor anti-B7.2 alone affected proliferation or cytokine production. However, administration of both anti-B7.1 and B7.2 completely inhibited proliferation as well as IL-2 and TNF-alpha production. CONCLUSIONS: B7.1 and B7.2 are expressed in the eye at different times during EAAU. Both B7 molecules are required for the induction of EAAU, although they probably have different roles.

Animals↗