scholarly journals INDUCTION AND REVERSAL OF IMMUNE PARALYSIS IN VITRO

1970 ◽  
Vol 132 (5) ◽  
pp. 845-857 ◽  
Author(s):  
V. S. Byers ◽  
E. E. Sercarz

Induction of the immune response can only be completed after antigen is removed from the cellular environment. Primed rabbit lymph node fragments were cultured in vitro with 5 mg/ml BSA. If antigen was removed from the fragments 2 hr later, they produced a normal anti-BSA response, which was first evident 5 days later. If antigen removal was delayed for 3 days, the onset of the response was postponed for 2 to 3 days. Pulses with BUDR marked the periods of cell proliferation in both sets of cultures, and established that the postponement of antibody production was preceded by a postponement in the wave of proliferation among precursors of antibody forming cells. The similarity in avidity of antibody-containing fluids from normal and postponed cultures support the idea that the same cell population produced the response in each case. It was concluded that a reversible state of paralysis could be instituted in antigen-responsive cells, and this state did not depend upon cell-killing. The widespread incidence of temporary paralysis as an early aspect of the immune response was discussed.

2021 ◽  
Vol 13 (578) ◽  
pp. eabg5638
Author(s):  
Gerald P. Morris

Development of a human lymphoid organoid system enables in vitro modeling of immune responses and antibody formation.


1974 ◽  
Vol 140 (5) ◽  
pp. 1245-1259 ◽  
Author(s):  
Ole Werdelin ◽  
Otto Brændstrup ◽  
Eskild Pedersen

We have studied the physical interaction between macrophages and lymphocytes during the immune response to purified protein derivative of tuberculin (PPD) in vitro. Mixtures of peritoneal macrophages and lymph node lymphocytes from guinea pigs immunized with tubercle bacilli formed cell clusters during 20 h of culture with PPD. The number of clusters produced was correlated to the number of immune lymphocytes in the cultures. Peritoneal macrophages which had been pulsed with PPD and untreated lymph node lymphocytes produced cell clusters in the absence of free PPD in numbers equivalent to those produced by the same cells in the presence of free PPD. In cultures containing a mixture of PPD-pulsed macrophages, not-pulsed macrophages, and immune lymphocytes with no free PPD, cell clusters developed mainly between the antigen-pulsed macrophages and lymphocytes. Cluster formation was antigen-specific with the specificity residing in the lymphocytes, mainly or exclusively in the T lymphocytes. These data indicate that in the process of cell cluster formation macrophages serve as antigen-binding (or -processing) cells, while a subpopulation of lymphocytes interact physically and specifically with the macrophages.


1972 ◽  
Vol 136 (2) ◽  
pp. 353-368 ◽  
Author(s):  
Alberto J. L. Macario ◽  
Everly Conway de Macario ◽  
Claudio Franceschi ◽  
Franco Celada

We have cultivated lymph node microfragments from ß-D-galactosidase (Escherichia coli) primed rabbits and have measured their secondary response directed towards the whole molecule (precipitating antibodies) and to a single determinant (activating antibodies) of the antigen. By decreasing the size of the fragments to 105 cells, we began to observe heterogeneity among identical cultures in terms of positivity of response, antibody specificity, and titers. The affinity of "early" activating antibodies was inversely proportional to the dose of challenge. While no maturation was seen in low and excessive challenge, in all cultures receiving intermediate doses the association constant was raised several orders of magnitude within periods of 20 days. The relevance of these data to the mechanism of affinity selection of antigen-sensitive cells is discussed.


2006 ◽  
Vol 203 (8) ◽  
pp. 1903-1913 ◽  
Author(s):  
Brian Webster ◽  
Eric H. Ekland ◽  
Lucila M. Agle ◽  
Susan Chyou ◽  
Regina Ruggieri ◽  
...  

Lymph nodes grow rapidly and robustly at the initiation of an immune response, and this growth is accompanied by growth of the blood vessels. Although the vessels are critical for supplying nutrients and for controlling cell trafficking, the regulation of lymph node vascular growth is not well understood. We show that lymph node endothelial cells begin to proliferate within 2 d of immunization and undergo a corresponding expansion in cell numbers. Endothelial cell proliferation is dependent on CD11c+ dendritic cells (DCs), and the subcutaneous injection of DCs is sufficient to trigger endothelial cell proliferation and growth. Lymph node endothelial cell proliferation is dependent on vascular endothelial growth factor (VEGF), and DCs are associated with increased lymph node VEGF levels. DC-induced endothelial cell proliferation and increased VEGF levels are mediated by DC-induced recruitment of blood-borne cells. Vascular growth in the draining lymph node includes the growth of high endothelial venule endothelial cells and is functionally associated with increased cell entry into the lymph node. Collectively, our results suggest a scenario whereby endothelial cell expansion in the draining lymph node is induced by DCs as part of a program that optimizes the microenvironment for the ensuing immune response.


1970 ◽  
Vol 132 (6) ◽  
pp. 1267-1278 ◽  
Author(s):  
Klaus-Ulrich Hartmann

The immune response to foreign erythrocytes was studied in vitro. Two subpopulations of cells were prepared. One was a population of bone marrow-derived spleen cells, taken from thymectomized, irradiated, and bone marrow-reconstituted mice; there was evidence that most of the precursors of the PFC had been present in this cell population, but few PFC developed in cultures of these cells alone in the presence of immunogenic erythrocytes. Another cell suspension was made from spleens of mice which had been irradiated and injected with thymus cells and erythrocytes; these cells were called educated T cells. The two cell suspensions together allow the formation of PFC in the presence of the erythrocytes which were used to educate the T cells, but not in the presence of noncross-reacting erythrocytes. If bone marrow-derived cells and T cells were kept in culture together with two different species of erythrocytes, and if one of the erythrocytes had been used to educate the T cells, then PFC against each of the erythrocytes could be detected.


1969 ◽  
Vol 130 (5) ◽  
pp. 1031-1045 ◽  
Author(s):  
Stuart F. Schlossman ◽  
Judith Herman ◽  
Arieh Yaron

Studies of the immunochemical specificity of antigen-induced thymidine-2-14C incorporation in lymph node cells obtained from animals immunized to a series of closely related α-DNP-oligolysines, ϵ-DNP-oligolysines, and oligolysines have shown that the sensitized cell exhibits an extraordinary degree of specificity for antigen. The sensitized cell is maximally stimulated by the homologous immunizing antigen and can discriminate among compounds which differ from one another only in the position of a dinitrophenyl group or D-lysine residue on an identical oligolysine backbone. These studies support the view that the immunogen is not degraded prior to the induction of the immune response, and that the majority of cells produced as a consequence of immunization have stereospecific antigen receptors for the DNP-oligolysine used to induce the response; a smaller and more variably sized population of cells is produced with receptors specific for the oligolysine portion of the immunizing antigen. When specifically sensitized lymph node cell cultures are stimulated in vitro by heterologous DNP-oligolysines, the oligolysine- and not the DNP-oligolysine-sensitive population of cells appears to play a crucial role in the specificity of such cross-reactions. It is concluded from these studies that the antigen receptor on the sensitized lymph node cell differs in both kind and degree from conventional antibody. The chemical nature of the receptor and the means by which this receptor reacts with antigen to initiate the biosynthetic or proliferative cellular immune response still remain undefined.


1963 ◽  
Vol 117 (6) ◽  
pp. 1053-1062 ◽  
Author(s):  
Thomas F. O'Brien ◽  
Maria C. Michaelides ◽  
Albert H. Coons

The in vitro anamnestic antibody response of popliteal lymph node fragments to additions of antigen closely resembles the in vivo anamnestic antibody response in its sensitivity to antigen, in the time course of antibody production, and in the sequence of appearance and the morphology of the antibody containing cells. Most of the cells responsible for antibody synthesis remain in the explant and do not migrate, although a few can be found in the outgrowing sheet of cells. The smallest concentration of bovine serum albumin which stimulates an anamnestic response in vitro is about 1 x 10–9 gm/ml.


2018 ◽  
Author(s):  
Franciele Carolina Silva ◽  
Vinicius Dantas Martins ◽  
Felipe Caixeta ◽  
Matheus Batista Carneiro ◽  
Graziele Ribeiro Goes ◽  
...  

AbstractAn association between increased susceptibility to infectious diseases and obesity has been described as a result of impaired immunity in obese individuals. It is not clear whether a similar linkage can be drawn between obesity and parasitic diseases. To evaluate the effect of obesity in the immune response to cutaneous L. major infection, we studied the ability of C57BL/6 mice submitted to a high fat and sugar diet to control leishmaniasis. Mice with diet-induced obesity presented thicker lesions with higher parasite burden and more inflammatory infiltrate in the infected ear when infected with L. major. We observe no difference in IFN-γ or IL-4 production by draining lymph node cells between control and obese mice, but obese mice presented higher production of IgG1 and IL-17. A higher percentage of in vitro-infected peritoneal macrophages was found when these cells were obtained from obese mice when compared to lean mice. In vitro stimulation of macrophages with IL-17 decreased the capacity of cells from control mice to kill the parasite. Moreover, macrophages from obese mice presented higher arginase activity. Together our results indicate that diet-induced obesity impairs resistance to L. major in C57BL/6 mice without affecting the development of Th1 response.Author SummaryThe obesity is a public health problem and it is reaching extraordinary numbers in the world and others diseases are being involved and aggravated as consequence of obesity. What we know is that some diseases are more severe in obese people than in normal people. We did not know how obesity changes the profile of immune response to infectious agents, leading to the more severe diseases. That‘s why we decided to investigate how obese mice lead with Leishmania major infection. Leishmaniasis is a protozoa parasite infection considered a neglected disease. To try our hypothesis we gave a hipercaloric diet to induce obesity in C57BL/6 mice. After that, we injected L. major in the mice ear and followed the lesion for 8 weeks. We observed a ticker lesion and the cells from draining lymph node from obese mice produced more IL-17 than cells from normal mice. We also infected in vitro, macrophages from obese mice and stimulated the cells with IL-17, and we observed that the macrophages from obese mice are more infected by the L. major and it is worst in the presence of IL-17. Our results suggest that diet induced obesity decrease the resistance to infection.


2006 ◽  
Vol 13 (1) ◽  
pp. 19-25 ◽  
Author(s):  
Erik L. Munson ◽  
Dean T. Nardelli ◽  
K. H. Kevin Luk ◽  
Monica C. Remington ◽  
Steven M. Callister ◽  
...  

ABSTRACT Determination of the immunological mediators responsible for promoting the production of borreliacidal antibody may facilitate the development of an improved borreliosis vaccine for human and veterinary use. Previously, we developed an in vitro assay to determine if borreliacidal antibody production could be augmented by treatment with different cytokines. In this study, in vitro treatment of lymph node cells producing borreliacidal antibody with recombinant interleukin-6 (rIL-6) resulted in a fourfold enhancement of anti-OspA borreliacidal antibody. Moreover, rIL-6 enhanced Western immunoblot titers and increased the number of B lymphocytes. In contrast, treatment of anti-OspA borreliacidal antibody-producing cells with anti-IL-6 resulted in a fourfold reduction in borreliacidal activity. Treatment with anti-IL-6 also inhibited enhanced borreliacidal antibody production induced by anti-gamma interferon. These data suggest that IL-6 plays a significant role in the production of anti-OspA borreliacidal antibodies.


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