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I N Targoff

Publications and source records attributed to I N Targoff.

60 records · Page 4Linked to original sources
PubMed1987

Measurement of antibody to Jo-1 by ELISA and comparison to enzyme inhibitory activity.

Antibody to the Jo-1 antigen (histidyl-tRNA synthetase) is found almost exclusively in myositis patients, usually those with adult PM, but has been found in only 30% of that group by immunodiffusion or other techniques thus far reported. We have reexamined the prevalence of antibody to Jo-1 in sera from 130 patients and 82 controls by using the sensitive ELISA technique. The ELISA used affinity-purified, enzymatically active bovine Jo-1 antigen. A wide range of antibody level by ELISA was found among 24 immunodiffusion positive sera. Six myositis and two control sera had apparent specific antibody detectable only by ELISA. Overall, however, the antibody continued to show high myositis specificity with predominance in adult PM (35.8% in that group). Because the antibody inhibits enzymatic activity of the synthetase antigen, we also studied the quantitative inhibitory activity of these sera to compare with the antibody activity as determined by ELISA. Twenty-four immunodiffusion-positive sera, 29 immunodiffusion-negative sera, and 15 normal sera were tested at 1/50 dilution in the reaction mixture. There was background inhibition by all normal sera tested that averaged 30.5%. All but one immunodiffusion negative myositis sera (a high binder by ELISA) inhibited less than 50% of the average with normal serum. Twenty-three of 24 immunodiffusion positive sera inhibited greater than 80% of this normal average; the other inhibited 66%. The serum dilution giving 50% inhibition was highly correlated (R = 0.83) with the ELISA activity. Thus, inhibition of histidyl-tRNA synthetase activity is a relatively accurate measure of Jo-1 antibody. This method should be applicable to measuring antibody to other aminoacyl-tRNA synthetases.

Amino Acyl-tRNA Synthetases↗
PubMed1985

The association between Mi-2 antibodies and dermatomyositis.

Antibodies to Mi, an antigen in calf thymus extract, have been demonstrated by complement fixation inhibition in polymyositis (PM) and dermatomyositis (DM) sera but not in the sera of individuals without myositis. The original Mi reference serum defined 2 precipitating antibodies, using immunodiffusion (ID). Anti-Mi-1 was not active in complement fixation. We have now studied in further detail anti-Mi-2, which appears to be the antibody in Mi serum that fixes complement. Mi-2 antigen was purified by immuno-affinity chromatography. An enzyme-linked immunosorbent assay (ELISA) to measure Mi-2 antibody, using this antigen, was used to test the sera of 139 myositis patients: 52 had DM and 87 had PM. Control sera from 35 normal subjects and 93 patients with other connective tissue diseases were also tested. Only 13 sera were considered definitely positive for anti-Mi-2. All were from patients who had myositis, 11 of whom had DM. Only DM sera had anti-Mi-2 by ID, and all sera with anti-Mi-2 by ID were positive by ELISA. A number of other sera, including many from patients with other connective tissue diseases and 2 from normal subjects (all without precipitating antibodies) had lower elevations which were of uncertain significance. Detection of anti-Mi-2 by ID as well as by ELISA was significantly more frequent in DM than in PM. Anti-Mi-2 appears to be closely linked to DM, and is the first specific serologic marker for this form of myositis.

Antibody Specificity↗
PubMed1983

Antibodies to Mi-1 in SLE: relationship to other precipitins and reaction with bovine immunoglobulin.

Precipitating antibodies to Mi-1, a protein antigen purified from calf thymus nuclear extract, have been reported in a small percentage of patients with dermatomyositis (DM) but not in patients with other connective tissue diseases or controls. Mi-1 shares certain characteristics with immunoglobulin, including the ability to react with rabbit anti-bovine immunoglobulin G (BIgG). A more extensive survey for anti-Mi-1 has been performed, involving 51 normal controls, 67 patients with polymyositis (PM) or DM, 47 patients with rheumatoid arthritis (RA), 41 SLE patients without any other precipitating antibodies to saline extractable tissue antigens on routine testing, and 247 patients, many with SLE, known to have other precipitins. Anti-Mi-1 was found in 13 patients from the latter group (5.25%) and two patients with PM or DM (3.0%), and was not found in other groups. It was found in seven of 95 (7.4%) with anti-nRNP, three of 32 (9.4%) with anti-Sm (with or without anti-nRNP) and three of 120 (2.5%) with anti-Ro (SSA). Anti-Mi-1 cross-reacts directly with BIgG but differs from ordinary rheumatoid factor in its frequent reaction with Fab2 fragments and restricted species specificity. Thus, anti-Mi-1 can be found in patients with diseases other than DM, including SLE, most often in patients with antibodies to nRNP.

Arthritis, Rheumatoid↗