scholarly journals ALLOANTISERUM-INDUCED INHIBITION OF MIGRATION INHIBITION FACTOR PRODUCTION IN IMMUNE RESPONSE GENE-CONTROLLED IMMUNE SYSTEMS

1974 ◽  
Vol 140 (2) ◽  
pp. 383-395 ◽  
Author(s):  
Shlomo Z. Ben-Sasson ◽  
Ethan Shevach ◽  
Ira Green ◽  
William E. Paul
Keyword(s):  
T Cell ◽  
Guinea Pigs ◽  
Opposite Effect ◽  
Cell Function ◽  
Migration Inhibition Factor ◽  
Immune Response Gene ◽  
Migration Inhibition ◽  
Inhibition Factor ◽  
Controlled Systems

We have previously demonstrated that alloantisera prepared by reciprocal immunization of strain 2 and strain 13 guinea pigs specifically block stimulation of in vitro DNA synthesis in genetically controlled systems. In order to determine whether this blockade extends to other T-lymphocyte functions, we examined the effect of alloantisera on the production of migration inhibition factor (MIF). (2 x 13)F1 guinea pigs were immunized with a DNP derivative of the copolymer of L-glutamic acid and L-lysine (DNP-GL) and with DNP guinea pig albumin (GPA). The response to the former is controlled by a 2-linked Ir gene while that to the latter is mainly controlled by a 13-linked Ir gene. MIF production was assayed by an indirect procedure in which the migrating cell population lacked the histocompatibility antigen against which the alloantiserum was directed. Our results showed that anti-2 serum blocked MIF production by F1 cells in response to DNP-GL but not DNP-GPA while anti-13 serum had the opposite effect. These experiments show that expression of a second major T-cell function is specifically blocked by alloantisera and suggest that Ir-gene products may act as antigen recognition substances on more than one type of T cell.

scholarly journals Regulation of granulomatous inflammation in murine schistosomiasis. In vitro characterization of T lymphocyte subsets involved in the production and suppression of migration inhibition factor.

1980 ◽  
Vol 151 (6) ◽  
pp. 1398-1412 ◽  
Author(s):  
S W Chensue ◽  
D L Boros ◽  
C S David
Keyword(s):  
T Cell ◽  
T Lymphocytes ◽  
Granulomatous Inflammation ◽  
Migration Inhibition Factor ◽  
Migration Inhibition ◽  
Spleen Cells ◽  
Inhibition Factor ◽  
Lymphokine Production

Host granulomatous inflammation in murine schistosomiasis mansoni is a T cell-mediated immune response, which, at the chronic stage of the disease, undergoes T suppressor lymphocyte-dependent modulation. In the present study this phenomenon was further analyzed in vitro. Spleen cells of mice undergoing modulation (20 wk of infection) when mixed with spleen cells of animals exhibiting vigorous granulomatous responses (8 wk of infection) abrogated in vitro migration inhibition factor (MIF) production by the latter. Characterization of the delayed-type hypersensitivity T lymphocytes involved in lymphokine production showed that they belonged to the Lyt-1+ subset and did not express I region-encoded antigens. In contrast, T lymphocytes involved in the suppression of MIF activity belonged to the Lyt-2+ subpopulation of cells, which expressed I-J- and I-C-subregion determinants. These results suggest that the modulation of the granulomatous hypersensitivity response in mice is the result of T-T cell interaction with subsequent regulation of inflammatory lymphokine production.

scholarly journals Requirement for T cells in the production of migration inhibitory factor.

1975 ◽  
Vol 142 (5) ◽  
pp. 1306-1311 ◽  
Author(s):  
B R Bloom ◽  
E Shevach
Keyword(s):  
T Cells ◽  
T Cell ◽  
B Lymphocytes ◽  
Cell Function ◽  
Plaque Assay ◽  
Quantitative Measure ◽  
Immune Response Gene ◽  
Migration Inhibition ◽  
Qualitative Assay ◽  
Gene Restriction

The question whether B lymphocytes are capable of being activated by antigen in the absence of functional T cells was investigated in a model that excludes participation of T cells by virtue of an immune response gene restriction. Strain 2 guinea pigs are capable of responding to immunization with DNP-PLL, whereas strain 13 animals are not. In the present experiments, animals of both strains were immunized with DNP-PLL complexed to ovalbumin (DNP-PLL-Ova) under conditions in which equal titers of antibodies to DNP were produced by both strains. The failure of T cells of strain 13 animals to respond to DNP-PLL was confirmed by the virus plaque assay. While spleen cells from both strains produced MIF after stimulation with DNP-PLL-Ova, in response to DNP-PLL only strain 2 spleens were able to produce MIF. Cells from neither strain could be activated by DNP-guinea pig albumin to produce MIF. We conclude that B lymphocytes are incapable of being stimulated by antigen in the absence of T cells, and that MIF production is a thymus-dependent response. While the results indicate that MIF production is a valid qualitative assay for T-cell competence, since MIF can be produced by B and T cells, the degree of migration inhibition cannot be regarded as a quantitative measure of T-cell function.

Suppression of migration inhibition factor (MIF) production by mitomycins in vitro

Immunobiology ◽  
1986 ◽  
Vol 172 (1-2) ◽  
pp. 120-127 ◽  
Author(s):  
J.M. Van Der Nat ◽  
J.xH. Beijnen ◽  
H. Van Dijk ◽  
W.J.M. Underberg ◽  
R.P. Labadie
Keyword(s):  
Migration Inhibition Factor ◽  
Migration Inhibition ◽  
Inhibition Factor

Cellular (T Cell) Immunity in the Human Newborn

PEDIATRICS ◽  
1979 ◽  
Vol 64 (5) ◽  
pp. 814-821
Author(s):  
E. Richard Stiehm ◽  
Harland S. Winter ◽  
Yvonne J. Bryson
Keyword(s):  
T Cell ◽  
Cell Function ◽  
Inhibition Factor ◽  
Susceptibility To Infection ◽  
Cell Immunity ◽  
Human Newborn ◽  
Occasional Occurrence ◽  
Cutaneous Hypersensitivity ◽  
Cellular Immune

The cellular immune system of the human newborn, like the rest of the immunologic apparatus, is anatomically intact, antigenically inexperienced, and functionally deficient. The latter is suggested by the newborns' enhanced susceptibility to infection, diminished delayed cutaneous hypersensitivity reactions, and selective abnormalities (when compared to adults) of measures of cellular immunity in vitro. These include impaired proliferative response to ubiquitous antigens, depressed lymphotoxin, migration inhibition factor, and immune interferon production, and diminished cytotoxic reactions including cell-mediated lympholysis. By contrast, other aspects of neonatal T cell function, such as to mitogens or allogeneic lymphocytes, natural interferon and leukocyte inhibition factor production, and number and percentage of E-rosette-forming cells are generally normal. These decreased functional properties may provide an explanation for the newborns' susceptibility to infection and for the occasional occurrence of engraftment of foreign cells from either the mother or from prenatal or neonatal blood transfusion.

scholarly journals Immune response gene control of determinant selection. I. Intramolecular mapping of the immunogenic sites on insulin recognized by guinea pig T and B cells.

1977 ◽  
Vol 145 (3) ◽  
pp. 726-742 ◽  
Author(s):  
M A Barcinski ◽  
A S Rosenthal
Keyword(s):  
T Cell ◽  
Guinea Pig ◽  
Guinea Pigs ◽  
Cell Function ◽  
Strain Differences ◽  
Amino Acid Sequences ◽  
Immune Response Gene ◽  
Antigenic Determinants ◽  
Histocompatibility Complex ◽  
A Chain

T-cell DNA synthesis and T-helper cell function in response to isolated insulin chains and naturally occurring insulin variants was assessed in insulin immune guinea pigs. Two distinct antigenic determinants, recognized by T cells, were defined. One localized in the B chain and the other one constituted by amino acids A8, A9, and A10 of the insulin A-chain loop. Recognition of the B-chain determinant is under the control of Ir genes linked to the strain 13 major histocompatibility complex. This was shown by studying the response to isolated insulin B chain in F1(2 x 13) guinea pigs, as well as serologically defined backcrosses and outbred animals. Insulin recognition through the A-chain loop determinant is specific for strain 2 guinea pigs. These animals recognize this region of the molecule even when displaying different amino acid sequences. The strain differences observed in those antigenic sites eliciting T-cell recognition was not found at an antibody level. No differences could be detected in the ability of the different insulin variants to inhibit the binding of 125I-labeled pork insulin to strain 2 guinea pig anti-pork insulin or to strain 13 guinea pig anti-pork insulin.

Sign in / Sign up

Export Citation Format

Share Document