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
1974 ◽  
Vol 140 (2) ◽  
pp. 383-395 ◽  
Author(s):  
Shlomo Z. Ben-Sasson ◽  
Ethan Shevach ◽  
Ira Green ◽  
William E. Paul

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.


1980 ◽  
Vol 151 (6) ◽  
pp. 1398-1412 ◽  
Author(s):  
S W Chensue ◽  
D L Boros ◽  
C S David

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.


1982 ◽  
Vol 68 (1) ◽  
pp. 39-46 ◽  
Author(s):  
Giorgio Cortesina ◽  
Giovanni Patrick Cavallo ◽  
Fabio Beatrice ◽  
Alberto Sartoris ◽  
Mario Bussi ◽  
...  

The production of leukocyte migration inhibition factor (LIF) from lymphocytes after stimulation with 3 M KCl soluble tumor and normal mucosa extracts was investigated in 30 patients with laryngeal carcinoma at different development stages and in 30 normal donors. The experiments were performed in heterologous and autologous systems. In heterologous systems 3 M KCl tumor extracts induced LIF production by heterologous lymphocytes from patients in 91 % of the cases, and normal mucosa extracts induced LIF production by heterologous lymphocytes from patients in 73 % of the cases and from normal donors in 90 % of the cases. In autologous systems 3 M KCl tumor extracts induced LIF production by autologous lymphocytes from the same patients in 65 % of the cases, whereas the normal laryngeal mucosa extracts induced LIF production by the same autologous lymphocytes in the 6 % of the cases. The high positivity percentage of the test in heterologous systems could be related to differences in the major histocompatibility complex. The 65 % test positivity in autologous systems using tumor extracts could be related to the presence of tumor associated antigens.


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