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PubMed1976

Studies on delayed hypersensitivity pleural exudates in guinea pigs. I. Demonstration of substances in the cell-free exudate which cause inhibition of mononuclear cell migration in vitro.

Leucocyte migration inhibitory (MI) activity was investigated in vitro in the delayed hypersensitivity reaction induced by intrapleural injection of PPD into FCA-sensitized guinea-pigs. During the initial reaction (6 h) two types of antigen-dependent MI activity were detected in serum and cell-free exudate. One was of high molecular weight and associated with immunoglobulin and the other was of low molecular weight and appeared to be related to so-called "antigen-dependent MIF". As the reaction progressed (i.e. 12-24 h), two types of antigen-dependent MI activity were revealed in exudate, but not in serum. One was high molecular weight and the other was low molecular weight and thought to be related to so-called "antigen-independent MIF". Similar experiments were performed on the reverse passive Arthus reaction in the pleural cavity of guinea-pigs. A high molecular weight MI activity was detected in 6-h cell-free exudate and was found to be antigen-independent. "So-called MIF" was not found in this reaction.

Animals↗
PubMed1976

Leucocyte migration inhibition factor (LIF) production by lymphocytes of normal children, newborns, and children with immune deficiency.

The reproducibility of a simplified, sensitive and rapid agarose-cell droplet assay for leucocyte migration inhibition factor (LIF) activity was studied. Removal of T cells with anti-T-cell serum eliminated LIF activity, indicating that in humans it is probably the T cell that produces LIF. Cord blood lymphocytes produce LIF, although spontaneous migration of leucocytes is less than in older children. The cause of this apparently does not reside in the PMN leucocytes. Studies of children with immunodeficiency suggest that the T-cell population in humans is heterogenous. B-cell deficiencies such as hypogammaglobulinaemia, have normal PPD and PHA induced LIF production, whilst some patients with ataxia-telangiectasia have defective PPD LIF activity, their PHA LIF activity being only minimally depressed. On the other hand, Down's syndrome patients with reduced blood T cells have remarkably deficient LIF activity to PHA and relatively good activity to PPD. Children receiving steroid therapy lose much of their ability to produce LIF to the specific antigen PPD, but not to the non-specific mitogen PHA.

Adolescent↗
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↗
PubMed1977

Analysis and function of T and B cells subpopulations in sarcoidosis.

Various technical procedure were applied to the purification of T and B lymphocytes subpopulation in sarcoidosis. Patients were selected according to the presence of a characterized deficit in cell-mediated immune functions. These purified lymphocytes populations were further analysed for their ability to release lymphokines in the presence of Con-A-sepharose or specific antigens. Among these factors, MIF, LIF and mitogenic factor (MF) were looked for. For the determination of MIF and LIF, a newly elaborated technique was deviced which allows a semi-quantitative approach of the lymphokine production. The following results were obtained: A decrease in the absolute number of T lymphocytes was observed among all our patients, and a increase in the number of Ig producing cells. A rather large percent (15 to 40%) of null cells which were carrying characteristic features of quiescent, non activable monocytes. The ability of T lymphocytes to release lymphokines was impaired in the presence of these monocytes but could be restored to normal levels when cells were removed. The results suggest that T cell function might be impaired, in sarcoidosis, by a non identified monocytes abnormal behaviour.

B-Lymphocytes↗
PubMed1978

Bacteria induce lymphokine synthesis polyclonally in human B lymphocytes.

We have studied the ability of various bacteria to stimulate human lymphocytes to produce leukocyte migration inhibitory factor (LIF). Mononuclear cells from adult and cord blood as well as purified T and B lymphocytes were stimulated with killed bacteria. The culture supernatants were tested for the presence of LIF by the agarose migration method. All nine bacterial strains tested activated unseparated mononuclear cells and B lymphocytes but not T cells to produce LIF. LIF was also present in cord blood cell cultures suggesting that the stimulation of lymphocytes was polyclonal rather than antigenic. Therefore, we propose that one of the physiologic functions of B lymphocyte lymphokines might be to form part of the nonspecific defense mechanisms against microbial invasion.

B-Lymphocytes↗