I L McLean

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UNLABELLED A spontaneous inflammatory disease in rats transgenic for HLA-B27 resembles the B27-associated human spondyloarthropathies. Colitis and arthritis, the two most important features, require T cells, gut bacteria, and high expression of B27 in bone marrow-derived cells. Control rats with HLA-B7 remain healthy. Most rats with HLA-Cw6 (associated with(More)
We postulate (Table I) that ReA is an antigen or immune complex induced condition caused by chronic intracellular bacterial infection at a distant site. The main predisposing factor is a failure to resist this infection. If the bacteria happen to carry MF, the inflammation is exacerbated in B27 positive patients. In contrast AS occurs in individuals who(More)
Immune responses to conserved, immunogenic homologues of the mycobacterial 65 kDa stress protein (SP65) have been implicated in inflammatory arthritis. Serum anti-SP65 was measured in AS, RA and healthy controls using an indirect enzyme immunoassay with recombinant SP65. IgA anti-SP65 was elevated in 19 of 59 AS patients, but the elevation in median level(More)
Sequence studies indicate that the alpha-1 domain of the HLA-B27 molecule has a characteristic unpaired cysteine residue at position 67, adjacent, because of secondary structure, to a lysine at position 70. Simple chemical considerations predict that this cysteine should have an exceptionally reactive sulphydryl group. We have shown by ELISA and flow(More)
Ankylosing spondylitis (AS) is strongly associated with possession of the HLA (Human Leucocyte Antigen)-B27 histocompatibility alloantigen. It is proposed that immunological tolerance to HLA-B27 allows the emergence of a lymphocyte clone with specificity for connective tissue antigens. Such a pathogenic clone would possess idiotypic determinants(More)
Immunoglobulin concentrates prepared from subjects of known HLA specificity were assayed for the presence of soluble HLA antigens by the inhibition of cytotoxic HLA alloantisera using a microabsorption procedure. The immunoglobulin preparations inhibited alloantisera of all specificities tested, regardless of the HLA type of the immunoglobulin donor,(More)
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