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PubMed1978

An in-vitro immunological assay for diagnosis of coeliac disease.

Production of leucocyte-migration-inhibition factor (L.I.F.) by peripheral-blood lymphocytes in response to challenge with gluten fractions was studied in 55 patients with coeliac disease and in 32 controls. 96% of the patients with coeliac disease demonstrated significant L.I.F. reaction in response to gluten fractions irrespective of their dietary status. Only 2 out of 32 controls had a positive reaction. This was in response to the B2 or B3 fraction, but never to both. The agarose microdroplet method of L.I.F. assay is reliable and technically simple enough for use in most clinical laboratories. The assay of L.I.F. production by peripheral-blood lymphocytes in response to gluten fractions, would be a useful adjunct in the diagnosis of gluten-sensitive enteropathy.

Adolescent↗
PubMed1978

Human migration inhibitory factor: purification and immunochemical characterization.

Using gel filtration and preparative isotachophoresis, the migration inhibitory factor (MIF) was highly purified from human lymphocytes activated with concanavalin A. MIF is an acidic protein with a mol wt of approximately equal to 25,000 daltons as determined by gel filtration and analytical polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate. The protein inhibits migration of macrophages in the capillary test and in addition, has a slowing effect on the electrophoretic mobility of guinea pig peritoneal macrophages. Rabbit antibodies specific for this protein, as determined by immunochemical techniques, neutralized the biological effect of MIF on migration and on the electrophoretic mobility of macrophages.

Antigen-Antibody Reactions↗
PubMed1976

The impact of HLA-A, B or HLA-D identity on the MIF production in MLC.

The relative influence on MIF release in MLC of different parts of the HLA region was studied in 1) MLCs between cells from HLA-A and B identical (probably HLA-D unidentical) unrelated persons and 2) MLCs between cells from HLA-D identical, HLA-A and B unidentical unrelated persons. It was found that the HLA-D part of the region has the major effect on the MIF production. Studies of MIF activity in supernatants from mitomycin treated cultures lent some evidence to the hypothesis that there is an extreme linkage disequilibrium between the HLA-D alleles and hypothetical separate MIF alleles. Examination of families with crossover between the HLA-A, B and HLA-D part of the region is required for confirmation of these findings.

Epitopes↗
PubMed1976

Some physicochemical properties of human leucocyte migration inhibitory factor (LIF).

Leucocyte migration inhibitory factor (LIF) obtained from human lymphocytes stimulated with concanavalin A was consistently and irreversibly blocked by the serine-esterase inhibitor phenyl-methyl sulphonylfuoride (PMSF). This effect was not due to fluoride ions, hydrolysis products of PMSF or to impurities. PMSF pulse treatment of human buffy coat cells did not affect cell migration under agarose. LIF was also irreversibly destroyed by treatment with L-cysteine and 2-mercapto-ethanol, suggesting that the molecule contains disulphide linkage groups decisive for its configuration and biological activity. Di-sodium EDTA completely inhibited LIF activity but only if present during the entire migration period. Removal of EDTA before LIF assay restored LIF activity. Leucotye migration was neighter influenced by L-cysteine nor by EDTA. LIF activity was slightly diminished after treatment at 56 degrees C for 1 h and completely lost at 80 degrees C for 1/2 h. Furthermore, LIF appeared rather stable when treated at pH values between 4 and 11. These findings suggest, but do not prove, an esterase or a protease nature of human LIF.

Concanavalin A↗
PubMed1975

Comparsion of the properties of two antigen-induced guinea pig lymphokines.

The properties of macrophage migration inhibition factor (MIF) and mitogenic factor (MF) were compared using culture supernatants of antigen-stimulated lymph node cells from inbred guinea pigs. Gel filtration on Sephadex G-100 indicated molecular weights of about 60,000 and 25,000 for MIF and MF, respectively. The lymphokines also differed with respect to heat sensitivity, MIF being largely inactivated by 60 degrees C for 20 min, whereas MF was unaffected by this treatment. The time course of production, antigen specificity of induction, and susceptibility to neuraminidase were also examined.

Animals↗
PubMed1977

New evidence that demonstrates that L-pro-L-leu-L-gly-NH2 might be the natural MIF.

A wide range of doses was used to study the effect of Pro-Leu-Gly-NH2 (MIF) on the MSH release in rat pituitaries incubated in vitro. The Pro-Leu-Gly-NH2 was added to one half of the gland, and the other was used as control. The MSH released into the medium was measured by a bioassay and the activity of the samples referred to a standard of synthetic alpha-MSH. Pro-Leu-Gly-NH2 in doses of 10 to 30 ng/ml inhibited the MSH release in about 60%. Doses between 10(3) to 10(4) ng/ml induced neither release nor inhibition of the release of MSH. Dose of 10(5) ng/ml clearly induced release of MSH. The results of the additional experiments presented, although they represent no proof, are in line with the contention that Pro-Ley-Gly-NH2 in the natural MIF.

Animals↗
PubMed1975

Human polymorphonuclear leucocyte migration inhibitory factor. Evidence for antigen dependency.

Sudies were performed on human polymorphonuclear leucocyte migration inhibitory factor (PMN-MIF) to determine its antigen dependence. PMN-MIF produced by lymphocytes in response to purified protein derivative or coccidiodin was measured in an agarose gel system with buffy coat leucocytes as indicator cells. PMN-MIF activity contained in the lymphocyte supernatants uniformly disappeared when the supernatants were diluted 1:50 with medium; the inhibitory activity was only restored when the diluted supernatants were reconstituted with specific antigen. PMN-MIF isolated by polyacrylamide gel electrophoresis showed the same properties as PMN-MIF present in whole supernatants. This factor consistently migrated in the albumin region on gel electrophoresis. These data indicate that human PMN-MIF is antigen-dependent.

Antigens↗
PubMed1977

Correlation between inhibition of indicator cell migration and tuberculin hypersensitivity in patients with suspected tuberculous inflammation of the uveal tissue.

Peripheral blood lymphocytes from patients with suspected tuberculous inflammation of the uveal tissue were examined for their capacity to produce in vitro a migration inhibition factor in the presence of specific antigen. Three modifications of the capillary tube migration technique were used to demonstrate MIF. The indicator cells were guinea pig peritoneal macrophages and human peripheral blood leucoytes. A correlation was found between the migration of indicator cells influenced by lymphocytes from Mantoux-positive donors in the presence of specific antigen and the tuberculin sensitivity. The possible uses of the in vitro tests as a correlate to cellular hypersensitivity in vivo in the human system are discussed.

Animals↗
PubMed1976

The immune response to oxidized ferredoxin. I. Specificity of the response to the amino terminal determinant.

Several synthetic peptide analogues of the amino terminal antigenic determinant (ala-tyr-lysile-ala-asp-ser) of oxidized ferredoxin (O-Fd) were tested for their ability to inhibit the complement fixation reaction between O-Fd and homologous rabbit antiserum, and to inhibit the migration of spleen cells from guinea-pigs immunized to O-Fd or to a conjugate of the amino terminal heptapeptide (N7) and bovine serum albumin (N7-BSA). The results of the migration inhibition assay suggest that the tetrapeptide and longer peptides of the native sequence were all recognized and stimulated the production of migration inhibition factor. Peptides modified at the aspartic residue were partially active while the serine modified peptide was not. Modification at the amino end of the heptapeptide had no effect on migration inhibition. As specificity controls, it was shown that the N7-BSA conjugate inhibited migration in O-Fd immunized animals, while O-Fd inhibited migration in N7-BSA immunized animals. The hexa-, hepta-, aspartic-deleted and serine-modified peptides were able to inhibit the complement fixation reaction with O-Fd and specific rabbit antiserum. Inhibition found with the serine-modified peptide and the lack of inhibition with the amino-modified peptide or the di-, tri-, tetra- and pentapeptides indicates the determinant recognized by the rabbit antibodies is either larger or is located nearer the middle of the heptapeptide than the determinant which induced the production of MIF.

Amino Acid Sequence↗
PubMed1977

Juvenile pernicious anemia associated with intestinal nodular lymphoid hyperplasia and immune deficiency state. Report of a case.

A 17-year-old girl with humoral immune deficiency state was observed, in whom pernicious anemia developed one year before her death. The patient died after a very severe diarrheal attack and respiratory tract infection. The necropsy revealed intestinal nodular lymphoid hyperplasia. The immunological evaluation showed depressed IgG and IgM concentration with lack of IgA, however in the patient's blood there were found B lymphocytes containing IgA immunoglobulin. On the effect of crude gastric antigen the patient's lymphocytes showed M.I.F. release, although there were no circulating autoantibodies.

Adolescent↗