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At least 73 records · Page 4Linked to original sources
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↗
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↗