Abstract:
Peptides having at least nine amino acid residues each including an amino acid sequence which corresponds to position p200-208 or p262-266 of the human acetylcholine receptor .alpha.-subunit, but differing therefrom by one or more amino acid substitutions, are disclosed. These peptides inhibit the proliferative response of human peripheral blood lymphocytes to the myasthenogenic peptides p195-212 and p259-271 and are suitable for treatment of subjects afflicted with myasthenia gravis.
Abstract:
Synthetic peptides of at least 12 and at most 30 amino acid residues comprising a sequence consisting of, or found within, a complementarity-determining region (CDR) found in the heavy or light chain of the human anti-DNA 16/6Id monoclonal antibody, or a sequence obtained by replacement and/or deletion and/or addition of one or more amino residues to said sequence, and salts, chemical derivatives and polymers of said peptides can be used for immunomodulation of systemic lupus erythematosus-associated responses.
Abstract:
Synthetic peptides based on a complementarity-determining region (CDR) of the heavy or light chain of a pathogenic anti-DNA monoclonal antibody that induces a systemic lupus erythematosus (SLE)-like disease in mice, and analogs, and salts and chemical derivatives thereof; dual peptides comprising two such peptides or analogs covalently linked to one another either directly or through a short linking chain; peptide polymers comprising a plurality of sequences of said peptide or analog thereof; and peptide polymers attached to a macromolecular carrier, are disclosed, and pharmaceutical compositions comprising them for the treatment of SLE in humans.
Abstract:
A method of treating systemic lupus erythematosus (SLE) in a subject are provided. The method comprise altering in cells of the subject activity and/or expression of at least one gene selected from the group consisting of Mpo, Ltf, Lcn, Camp, Ngp, Slfn, Ctsg, Thbs1, S100a8, 1190003K14Rik, Prtn3, S100a9, Tfpi, Fzd6, Nid1, 5830484A20Rik, 5830484A20 LOC 545340, Tnfsf4, IPstpip2, Pigr, 270022B06Rik, L5R-alpha, A130040M12Rik, Gpr132, Cd8b1, Dhx9, Cyp11a1, Lmo7, Rnf184, Pstpip2, Hdgfrp3, Ass1 and Zbtb20, thereby treating SLE. Also provided are methods of diagnosing SLE and monitoring treatment of SLE.
Abstract translation:提供了一种治疗受试者系统性红斑狼疮(SLE)的方法。 该方法包括在细胞中改变选自Mpo,Ltf,Lcn,Camp,Ngp,Slfn,Ctsg,Thbs1,S100a8,1190003K14Rik,Prtn3,S100a9,Tfpi中的至少一种基因的至少一种基因的表达和/ ,Fzd6,Nid1,5830484A20Rik,5830484A20 LOC 545340,Tnfsf4,IPstpip2,Pigr,270022B06Rik,L5R-α,A130040M12Rik,Gpr132,Cd8b1,Dhx9,Cyp11a1,Lmo7,Rnf184,Pstpip2,Hdgfrp3,Ass1和Zbtb20,从而治疗SLE。 还提供诊断SLE和监测SLE治疗的方法。
Abstract:
Synthetic peptides of at least 12 and at most 30 amino acid residues comprising a sequence consisting of, or found within, a complementarity-determining region (CDR) found in the heavy or light chain of the human anti-DNA 16/6Id monoclonal antibody, or a sequence obtained by replacement and/or deletion and/or addition of one or more amino residues to said sequence, and salts, chemical derivatives and polymers of said peptides can be used for immunomodulation of systemic lupus erythematosus-associated responses.
Abstract:
The present invention provides methods for treating autoimmune diseases in mammals and for preventing or treating transplantation rejection in a transplant recipient. The methods of treatment involve the use of drugs capable of suppressing expression of MHC Class I molecules. In particular the use of the drug methimazole to suppress expression of MHC Class I molecules in the treatment of autoimmune diseases and the prevention or treatment of rejection in a transplant recipient is disclosed. In addition in vivo and in vitro assays are provided for the assessment and development of drugs capable of suppressing MHC Class I molecules.
Abstract:
The present invention provides methods for treating autoimmune diseases in mammals and for preventing or treating transplantation rejection in a transplant recipient. The methods of treatment involve the use of drugs capable of suppressing expression of MHC Class I molecules. In particular the use of the drug methimazole to suppress expression of MHC Class I molecules in the treatment of autoimmune diseases and the prevention or treatment of rejection in a transplant recipient is disclosed. In addition in vivo and in vitro assays are provided for the assessment and development of drugs capable of suppressing MHC Class I molecules.
Abstract:
As assay for the measurement of direct binding of a peptide that is a T-cell epitope to gene products of the major histocompatibility complex (MHC), classes I and II, on the surface of intact living antigen-presenting cells, is provided. The assay comprises incubating the labelled peptide with the cells, and monitoring the extent of binding by the addition of a probe that reacts with the ligand used to label the peptide. The assay is suitable for autoimmune diseases and other immunological disorders. Peptides having a sequence corresponding to a stretch of the sequence of the antigen relevant to an immunological disorder, or modifications thereof, which bind to gene products of MHC, but do not stimulate T-cells, are also useful for the treatment of said disorders.