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

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.

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.


1979 ◽  
Vol 14 (4) ◽  
pp. 441-448 ◽  
Author(s):  
Richard H. Weisbart ◽  
David W. Golde ◽  
Leonard Spolter ◽  
Peter Eggena ◽  
Heinrich Rinderknecht

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

1980 ◽  
Vol 30 (3) ◽  
pp. 674-677
Author(s):  
K K Colburn ◽  
L G Wong ◽  
R F Ashman ◽  
R Wistar ◽  
R H Weisbart

Staphylococcal protein A is a bacterial cell wall product that binds human immunoglobulin G and thereby interferes with opsonization and phagocytosis of Staphylococcus aureus by neutrophils. Phagocytic cells are also responsive to various non-immunoglobulin lymphocyte mediators. We utilized the detection of a newly recognized mediator, a neutrophil migration inhibition factor from T-lymphocytes (NIF-T), to show that aggregates of staphylococcal protein A and immunoglobulins G could inhibit the responsiveness of neutrophils to NIF-T. That such aggregates may alter the responsiveness of neutrophils to lymphocyte mediators that amplify or modulate phagocytic functions may have important pathogenetic implications in staphylococcal infection.


1981 ◽  
Vol 3 (2) ◽  
pp. 179-185 ◽  
Author(s):  
Lawrence G. Wong ◽  
Keith K. Colburn ◽  
Amelia Kacena ◽  
Richard H. Weisbart

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