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T D Kinsella

Publications and source records attributed to T D Kinsella.

At least 37 records · Page 2Linked to original sources
PubMed1986

The detection of autoantibodies on HEp-2 cells using an indirect immunoperoxidase kit (Colorzyme).

An indirect immunoenzyme (IIE) kit to detect autoantibodies in the sera of patients with systemic rheumatic diseases has been evaluated and compared to a conventional indirect immunofluorescence (IIF) assay. Both IIF and IIE were performed on a human epithelial cell line (HEp-2) using sera categorized on the basis of their autoantibody specificity. The correlation coefficient between the two assays was greater than 0.77 for all autoantibodies except antimitochondrial antibodies, which had higher end-point titers with the IIE kit. The inter- and intratest variability of IIE and IIF was comparable, differing by no more than one tube dilution. The IIE test had less background staining, allowing for better resolution and easier interpretation of staining patterns. IIE assay in the form of a commercially available kit is a reliable alternative to IIF.

Autoantibodies↗
PubMed1985

Antinuclear, anticytoplasmic, and anti-Sjogren's syndrome antigen A (SS-A/Ro) antibodies in female blood donors.

A study of 2500 sera from female blood donors between the ages of 20 and 50 years was undertaken to determine the frequency of antinuclear (ANA), anticytoplasmic (ACA), and antimitochondrial (AMA) antibodies. When sera were tested by immunofluorescence (IF) on HEp-2 cells, 15.9 and 1.1% had ANA titers greater than 1/20 and 1/80, respectively. Analysis of these sera for autoantibody specificity showed: 1.5% antinucleolar, 1.0% anti-nuclear matrix, 0.2% anti-mitotic spindle apparatus, and 0.2% anti-primary biliary cirrhosis nuclear antigen. AMA titers of greater than 1/80 were seen in 2.5% and AMA titers greater than 1/160 were seen in 1.0%. None of the sera had anti-double stranded DNA. Testing of an additional 2500 sera for anti-Sjogren's Syndrome antigen A (anti-SS-A/Ro) revealed a frequency of 22/5000 (0.44%) with the highest frequency (0.72%) being in the 45-50 age group and a relatively high frequency (0.58%) in the 20-24 age group.

Adult↗
PubMed1984

Hereditary hemorrhagic telangiectasia versus CREST syndrome: can serology aid diagnosis?

Because the telangiectasia of hereditary hemorrhagic telangiectasia (HHT) and the CREST variant of scleroderma may be indistinguishable, we have tested the sera of eight patients with HHT for the presence of antinuclear (ANA) and anticentromere antibodies (ACA). In contrast to patients with the CREST syndrome, none of the sera of patients with HHT had elevated levels of ANA and a search for ACA was negative. Therefore, the presence of ACA may help differentiate the patient with CREST from the patient with HHT.

Adult↗
PubMed1984

Absence of impaired lymphocyte transformation to Klebsiella spp. in ankylosing spondylitis.

We have evaluated claims that impaired peripheral blood lymphocyte (PBL) transformation can occur with Klebsiella spp. in patients with ankylosing spondylitis (AS). PBL of four AS patients were cultured in vitro with autogenous faecal klebsiella, as were the PBL of age (+/- 3 years) and sex-matched pairs of 15-20 AS and normal controls cultured with heterogeneous AS-derived klebsiella and control bacterial isolates. Three of four AS patients responded to their own isolates, and no significant differences were found between the matched pairs in response to heterogeneous klebsiella isolates, including K21. Our studies did not show impaired PBL transformation with klebsiella in AS and therefore do not support claims of antigenic cross-reactivity between klebsiella and HLA-B27.

Cells, Cultured↗
PubMed1984

Antibodies from patients with autoimmune disease react with a cytoplasmic antigen in the Golgi apparatus.

In this study we report the identification of an antibody in the sera of some patients with autoimmune disease that reacted with a cytoplasmic antigen localized within the Golgi apparatus. The antibody reacted with all tissues investigated, which included pancreas, kidney, testis, liver, thymus, and spleen. In addition, it reacted with some human peripheral circulating lymphocytes, murine peritoneal macrophages, and a variety of tissue culture cell lines, which included HEp-2 cells (human epithelial carcinoma), baby hamster kidney cells, a canine thymus cell line, a primary kidney cell line, Ehrlich ascites cells, Wil-2 cells, and Raji cells. The antigen is located in the same region stained by the histochemical reaction for thiamine pyrophosphatase, thus indicating that the antigen is located within the Golgi apparatus. The antigen was not demonstrated by immunodiffusion of saline extracts of rabbit thymus, pancreas, or liver. The antigen in HEp-2 cells was resistant to RNase A, DNase I, micrococcal nuclease, and to extraction with 0.1 N HC1, but was sensitive to trypsin and Proteinase K. Eight patients with anti-Golgi antibodies have been identified. Six of the eight had systemic lupus erythematosus. Autoantibodies to a Golgi apparatus antigen might serve as a useful biologic marker to study the functional relationship of the Golgi apparatus to lymphocytes and macrophages.

Adult↗
PubMed1983

Clinical features of patients with antibodies directed against proliferating cell nuclear antigen.

The clinical and serologic features of 7 patients whose sera contained antibodies directed against proliferating cell nuclear antigen (anti-PCNA) were studied. Five of the patients had systemic lupus erythematosus (SLE), 1 had idiopathic diffuse proliferative glomerulonephritis, and 1 had seronegative arthritis. In a study of various rheumatic diseases, anti-PCNA was found in 2% of SLE sera but was not found in the sera of 100 rheumatoid arthritis patients, 20 mixed connective tissue disease patients, or 50 diffuse scleroderma patients. Patients with anti-PCNA had no history of hemolytic anemia, leukopenia, thrombocytopenia, or pleuro-pericarditis. Evidence that the production of anti-PCNA antibodies is sensitive to corticosteroid therapy is also presented.

Adult↗
PubMed1983

Immunocytological studies of Epstein-Barr viral antigen and antibody in rheumatoid synovial fluids.

Evidence for intra-articular immunity to Epstein-Barr virus (EBV) was sought in synovial fluids (SF) and SF phagocytes derived from patients with and without rheumatoid arthritis (RA). Antibody titres to EBV were not significantly different in SF of 32 RA and 25 non-RA patients. Whereas the majority of RA patients (69%) showed Ig-containing complexes (IC) in SF phagocytes, fluorescent antibody staining of these by anti-EBV serum was negative except with 6 RA patients. Extended analysis of the SF phagocytes of the latter, however, showed no EBV specificity in their IC, suggesting that these represented non-specific "pseudo-IC'. These studies do not support a role for EBV-containing IC in the propagation of rheumatoid synovitis and demonstrate that not all immunofluorescent inclusions in RA phagocytes (ragocytes) represent immune complexes.

Antibodies, Viral↗
PubMed1982

Studies of circulating immune complexes in ankylosing spondylitis.

Circulating immune complexes (CIC) were sought, by a fluorescent antibody immunophagocytosis (FIP) assay, in the sera of 30 patients with ankylosing spondylitis (AS), 62 with rheumatoid arthritis (RA), 27 with systemic lupus erythematosus (SLE) and 67 normal controls. Component analysis of CIC revealed significant elevations of total immunoglobulin (TIg), IgM and C3 for all patient study groups. In contrast to RA and SLE, CIC in AS sera contained significantly increased IgA and decreased IgG components. Categorization of AS patients as Grade I (mild disease) or Grade II (moderate/advanced disease) revealed no significant differences between the 2 groups in mean serum levels, component composition or prevalence of CIC. These results confirm the occurrence of CIC in AS but do not clarify the pathogenetic influence, if any, of CIC in this disease.

Adolescent↗
PubMed1981

Population studies of leukocyte-reactive antinuclear antibody and HLA antigens.

The prevalence of serum leukocyte-reactive antinuclear antibody (LR-ANA) was determined in 31 patients with ankylosing spondylitis (AS), their age-and gender-matched normal controls, and two tribes of 340 West Coast Canadian Indians (Bella Coolas and Haidas). At a serum dilution of 1 : 10, the prevalence of LR-ANA in AS and controls was 45% and 7%, respectively. At 1 : 20 dilution, the prevalence was 23% in AS, 0% in controls, 29% in Bella Coolas and 27% in Haidas. No concordance was found among LR-ANA, HLA-B27 and CREG-B7, and nine HLA-A and seven HLA-B antigens in the Indian tribes. These studies confirm an increased prevalence of LR-ANA in AS and AS kindreds, but the latter association appears to be independent of HLA antigens.

Antibodies, Antinuclear↗
PubMed1980

The CREST syndrome: a distinct serologic entity with anticentromere antibodies.

The CREST syndrome is a variant of systemic sclerosis characterized by the presence of calcinosis. Raynaud's phenomenon, esophageal motility abnormalities, sclerodactyly and telangiectasia. The serums of 27 patients with the CREST syndrome have been examined for the presence of antinuclear antibodies. Twenty-six of 27 (98 percent) serums contained high titers (> one:80) of an antibody that produces a discrete speckled pattern of immunofluorescence on a human laryngeal carcinoma cell line (HEp-2). The antibody has been shown to react with the centromeric region of metaphase chromosomes. This antibody was also found in three of 14 patients with Raynaud's disease, in one of 60 patients with systemic lupus erythematosus, in three of 26 patients with systemic sclerosis with diffuse scleroderma and in one of 15 patients with mixed connective tissue disease. The antibody was not detected in the serums of patients with rheumatoid arthritis. Sjögren's sicca complex or linear scleroderma. Patients with osteoarthritis who were age- and sex-matched to the group with the CREST syndrome did not have anticentromere antibodies. Autoantibodies found in other connective tissue diseases (anti-DNA, anti-RNP, Sjögren's syndrome antigen B (anti-SS-B) were not found in serums from patients with the CREST syndrome. A case report illustrating the appearance of the anticentromere antibody at a time when Raynaud's phenomenon antedated the clinical diagnosis of CREST syndrome is presented.

Adult↗
PubMed1977

Increased frequency of leukocyte-reactive antinuclear antibody in patients with ankylosing spondylitis.

Immunofluorescent studies were conducted for leukocyte-reactive antinuclear antibody (LR-ANA) with sera from 125 patients with ankylosing spondylitis (as), 124 with rheumatoid arthritis (RA) 74 with miscellaneous immune disorders (MID), 34 with acute inflammatory disorders (AID) and 122 non-immune controls. Positive reactions occurred with 60% of AS patients, 47% of RA, 40% of MID, 12% of AID, and 9% of non-immune controls. LR-ANA in AS sera invariably showed a homogeneous pattern of immunofluorescent staining with human granulocytes, occasionally reacted with human lymphocytes but did not react with other human and non-human substrates. Studies of 61 members of seven families with 18 cases of AS revealed a frequency of 38% LR-ANA, 30% AS and 55% HLA-B27, but no correlations were found among these parameters. These studies provide evidence of altered humoral immunity to human nucleic acids in the majority of patients with AS.

Adolescent↗
PubMed1976

Transformation of human lymphocytes in vitro by autologous and allogeneic rheumatoid synovial fluids.

To assess the possible participation of cellular immune mechanisms in the pathogenesis of rheumatoid arthritis (RA) in vitro studies of the blastogenicity of rheumatoid and non-rheumatoid synovial fluids for human peripheral blood lymphocytes were conducted. In autologous cultures it was found that 13 of 19 rheumatoid fluids induced significant lymphocyte blastogenesis, whereas only 1 of 13 nonrheumatoid fluids induced such a response. In allogeneic cultures rheumatoid fluids induce significant blastogenesis of RA lymphocytes in 18 of 23 experiments, and of non-RA lymphocytes in 8 of 18 experiments. By contrast, nonrheumatoid fluids induced significant blastogenesis of RA lymphocytes in 2 of 13 experiments, and of non-RA lymphocytes in 1 of 14 experiments. The blastogenicity of fluids was found to correlate significantly with the presence therein of immunofluorescent intracellular inclusions of immunoglobulin and complement. These studies support the concept that the presence of immune complexes in the majority of rheumatoid synovial fluids might render the latter blastogenic for human lymphocytes in vivo, thereby perpetuating rheumatoid synovitis.

Arthritis, Rheumatoid↗
PubMed1975

Perturbations of humoral and cellular immunity in a patient with pigmented villonodular synovitis.

Several parameters of the immune system have been studied in a patient with pigmented villonodular synovitis. Numerous immunoglobulin-synthesizing cells were found by immunofluorescent technics in both synovium and synovial fluid. Phytohemagglutinin-induced in vitro blastogenesis of peripheral blood T lymphocytes was absent whereas B-lymphocyte blastogenesis was preserved. These results indicate a necessity for evaluating immune responsiveness in other patients with pigmented villonodular synovitis.

Animals↗
PubMed1975

Serum complement and immunoglobulin levels in sporadic and familial ankylosing spondylitis.

Serum levels of C4, C3, IgG, IgM and IgA were measured by immunodiffusion in age matched groups of 48 sporadically encountered patients with ankylosing spondylitis, 56 with rheumatoid arthritis and 52 normal controls. Mean levels of C4 and IgA were significantly elevated in the sera of patients with sporadic ankylosing spondylitis, in comparison to normal controls. Mean IgA levels were also significantly elevated in 11 HL-A 27 positive patients with familial spondylitis but no such elevation was found in the sera of their healthy first-degree relatives with and without HL-A 27. The results of these studies suggest that humoral immune mechanisms may be involved in the pathophysiology of ankylosing spondylitis.

Adult↗
PubMed1974

Cardiovascular manifestations of ankylosing spondylitis.

The incidence of cardiovascular lesions in 97 patients with ankylosing spondylitis (AS) was found to be 14%; 8 patients had isolated aortic insufficiency (AI), 3 had isolated heart block, 2 had combined AI and heart block, and 1 had mitral insufficiency. In comparison with control groups of 81 patients with rheumatoid arthritis and 99 random hospital patients there was no increased incidence of isolated heart block in patients with AS. Clinical and postmortem findings indicated that the cardiovascular lesions of some patients with AS may antedate articular disease and may regress spontaneously. In addition, the unusual occurrence of AI in two patients with psoriatic spondylitis and in one with AS and regional enteritis is documented.

Aortic Valve Insufficiency↗
PubMed1974

Enhancement of human lymphocyte transformation by aggregated human gamma globulin.

The effect of heat-aggregated human gamma globulin (aggFII) on the induction of in vitro lymphocyte transformation, measured by the uptake of tritiated thymidine into newly synthesized DNA, was studied with peripheral blood lymphocytes derived from 12 patients with rheumatoid arthritis (RA), six with ankylosing spondylitis (AS), two with systemic lupus erythematosus (SLE), and seven normal subjects. It was found that 200 mug aggFII induced significant transformation of the lymphocytes of eight patients with RA, five with AS, one with SLE, and one normal subject. Neither deaggregated FII nor heat-aggregated human serum albumin induced significant transformation of the lymphocytes of any subject tested. A source of complement appeared necessary to support aggFII-induced blastogenesis, since enhanced transformation occurred only in the presence of fresh plasma. Heat-inactivated plasma and fetal calf serum (FCS), and FCS devoid of hemolytic complement, failed to support enhanced blastogenesis in the presence of aggFII. Since substrates similar to those employed in these studies are present in vivo in the rheumatoid joint, it is suggested that aggFII may enhance intra-articular lymphocyte transformation in subjects with RA.

Animals↗