INTERACTION IN VITRO BETWEEN RAT MACROPHAGES AND THORACIC DUCT LYMPHOCYTES DURING INITIATION OF ANTIBODY RESPONSES TO SHEEP ERYTHROCYTES

1970 ◽  
Vol 48 (5) ◽  
pp. 551-562 ◽  
Author(s):  
PJ McCullagh
1967 ◽  
Vol 168 (1012) ◽  
pp. 229-243 ◽  

The haemolysin response of rats to an intravenous dose of 10 8 sheep erythrocytes was abolished by pretreatment with 500 rad of whole body X-irradiation. The immunological deficiency in such animals could be corrected equally well by either an injection of thoracic duct cells or by an inoculum consisting almost exclusively of small lymphocytes, obtained in each case from normal (non-immune) rats. The reversal of unresponsiveness depended upon the survival of the donor lymphocytes in the X-irradiated recipients and was not due to a non-specific restoration of the hosts’ own capacity to form antibody. Evidence for this conclusion came from experiments in which the X-irradiated recipients were themselves immunologically tolerant of sheep erythrocytes; additional support came from the inability of lymphocytes from immunologically tolerant donors to restore specific responsiveness in X-irradiated (non-tolerant) recipients. In a proportion of trials the immunological tolerance to sheep erythrocytes exhibited by thoracic duct lymphocytes from tolerant donors could be broken by incubating the cells in vitro before their injection into X-irradiated recipients. This points to the existence of individual tolerant cells in the tolerant populations of lymphocytes. Taken as a whole the experiments suggest strongly that small lymphocytes are the precursors of the cells which produce haemolysin against sheep erythrocytes in the rat.


1972 ◽  
Vol 135 (5) ◽  
pp. 1049-1058 ◽  
Author(s):  
Marc Feldmann

The requirement for macrophages in thymus-dependent antibody responses was studied in vitro. Three different macrophage-deficient cell populations were studied: spleen cells passed through a glass bead column at 37°C, spleen cells cultured with specific antimacrophage serum, and thoracic duct lymphocytes. These cell populations from mice primed to dinitrophenylated (DNP) fowl gamma globulin were unable to respond to the homologous conjugate in vitro. DNP-reactive B cells were present in normal proportions, since all three macrophage-depleted populations responded normally to macrophage-independent and thymus-independent DNP flagella. Carrier-reactive T cells were present, as the helper capacity of carrier-primed spleen cells was the same as carrier-primed lymphocytes, and thoracic duct lymphocytes are a well-established source of helper cells. The inhibition of the cooperative response was thus due to removal of macrophages, and this was proven by restoration of thymus-dependent anti-DNP responses by small numbers of anti-θ-treated peritoneal exudate cells. These results suggest that macrophages are essential in cell collaboration, While their exact function in cell collaboration is not yet known, the above observation suggests that the mechanism of T-B collaboration involves the surface of macrophages.


1966 ◽  
Vol 124 (5) ◽  
pp. 1017-1030 ◽  
Author(s):  
James L. Gowans ◽  
Jonathan W. Uhr

Lymphocytes were obtained from the thoracic duct of rats 1½ to 15 months after primary immunization with a single dose of bacteriophage ϕX 174. An intravenous injection of these lymphocytes conferred on heavily X-irradiated rats the ability to form antibody in a secondary-type manner after a first injection of ϕX. Negligible responses were obtained after cell transfer if the recipients were not challenged with antigen. Thoracic duct cells from some immunized donors were incubated in vitro for 24 hr before transfer in order to destroy selectively the large, dividing lymphocytes. The responsiveness conferred on X-irradiated recipients by such "incubated" inocula was then compared with that given by equal numbers of "fresh" thoracic duct cells. In all such comparisons the recipients of the "incubated" cells gave higher and more rapid antibody responses. It was concluded that the cells in thoracic duct lymph which carried immunological memory were small lymphocytes.


1974 ◽  
Vol 140 (4) ◽  
pp. 921-938 ◽  
Author(s):  
Carl W. Pierce ◽  
Judith A. Kapp ◽  
Susan M. Solliday ◽  
Martin E. Dorf ◽  
Baruj Benacerraf

The effects of alloantisera against leukocyte alloantigens on plaque-forming cell (PFC) responses to sheep erythrocytes and the terpolymer of L-glutamic acid60-L-alanine30-L-tyrosine10 (GAT) by mouse spleen cells in vitro have been investigated. Polyspecific antibodies against both H-2 and non-H-2 alloantigens on responding spleen cells suppressed both IgM and IgG PFC responses; antisera against alloantigens coded for by the K and I regions, but not the D region, of the H-2 complex also effectively suppressed PFC responses. The suppression was not due to cytotoxicity to the spleen cells or anti-immunoglobulin activity in the sera and was directly related to the amount of antiserum added to the cultures. The suppression was specific for spleen cells against which the alloantiserum was directed. The alloantisera suppressed responses most effectively when present during the first 24 h of incubation, and although not rendering lymphoid cells incapable of developing PFC responses after removal of noncell-bound antibody, did act by interfering with successful initiation of the PFC response. The alloantisera suppressed both IgM and IgG PFC responses when directed against alloantigens only on macrophages, but selectively suppressed IgG responses when directed against alloantigens only on lymphoid cells. The alloantisera did not interfere with the ability of macrophages to bind GAT or to support the viability of the lymphoid cells, but did interfere with the ability of macrophage-associated antigen to effectively stimulate antibody responses by the lymphoid cells. Possible mechanisms for the effects of alloantisera on macrophages and the selective suppression of IgG responses when the antisera are directed against alloantigens on lymphoid cells are discussed with reference to our current understanding of genetic restrictions governing cell interactions in the development of antibody responses in mice.


1972 ◽  
Vol 135 (6) ◽  
pp. 1301-1315 ◽  
Author(s):  
Hans-Hartmut Peter ◽  
Joseph D. Feldman

Cell-mediated cytotoxicity (CMC) in spleens and lymph nodes of allografted rats was determined by release of 51Cr from labeled target cells incubated with aggressor lymphoid cells. CMC was first detected in grafted adult rats on day 5, peaked on days 7 and 8, and declined rapidly to background levels by days 9 to 11. In allografted neonates and in cyclophosphamide-treated or neonatally thymectomized adults CMC was a fraction of that observed in normal adult rats. Enhancing antibodies deferred in vivo peak activity of CMC in allografted neonates for 3–4 days, and blocked in vitro the action of aggressor lymphocytes by binding to target cells. Enhancing antibodies had no effect on the cytotoxicity of aggressor cells, but horse antibodies to rat thoracic duct cells inhibited in vitro CMC of aggressor cells.


1988 ◽  
Vol 10 (8) ◽  
pp. 919-924 ◽  
Author(s):  
Maria L. Villa ◽  
Francesca Valenti ◽  
Marina Mantovani ◽  
Franco Scaglione ◽  
Enrico Clerici
Keyword(s):  

1980 ◽  
pp. 1857-1885 ◽  
Author(s):  
P. Erb ◽  
M. Feldmann ◽  
R. Gisler ◽  
Barbara Meier ◽  
Angelika Stern ◽  
...  

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