Soluble Immune Response Suppressor (SIRS) Mediated Inhibition of Cell Division

1987 ◽  
pp. 47-58
Author(s):  
Thomas M. Aune
Keyword(s):  
Immune Response ◽  
Cell Division

A study of the adoptive secondary response to a protein antigen in mice

1961 ◽  
Vol 154 (956) ◽  
pp. 398-417 ◽  
Keyword(s):  
Immune Response ◽  
Cell Division ◽  
Antibody Production ◽  
Passive Immunization ◽  
Active Immunization ◽  
Lymphoid Cells ◽  
Protein Antigen ◽  
Secondary Response ◽  
Recipient Mouse ◽  
Time Control

An attempt has been made to study the cellular inheritance of the induced state of cellular differentiation associated with a secondary immune response. Lymphoid cells have been transferred from donor mice immunized against a protein antigen (bovine gamma globulin) into lethally X -irradiated recipients of the same inbred strain. Evidence is discussed which has led to the assumption that the cells capable of producing a secondary response divide in an irradiated environment. The experiments described here have been designed to show the effect of cell division on the capacity of these cells to produce antibody. The rate of anti­body production in an immune response has been measured by means of the antigen-elimina­tion technique. This technique has been calibrated in passive immunization experiments using an antiserum prepared in outbred mice. The amount of division by the transferred immunized cells before challenge was varied in two ways. First, mice were challenged at different intervals after the transfer of the same number of immunized cells into each recipient mouse. Secondly, different numbers of cells were injected into mice, and these left for a time sufficient for the smallest inoculum used to recolonize the host completely. In the first type of experiment, the results showed that the capacity to produce a secondary response steadily declined with increasing time. Control experiments showed that such a decline can occur after active immunization in non-irradiated mice. In the second type of experiment, the rate of antibody production was directly proportional to the size of the original inoculum of immunized cells. It seems that the rate of antibody production is not increased by cell division. The results are prob­ably, therefore, incompatible with those hypotheses which postulate that all of the mechan­ism responsible for antibody synthesis is capable of replication.

scholarly journals Widespread dysregulation of long non-coding genes associated with fatty acid metabolism, cell division, and immune response gene networks in xenobiotic-exposed rat liver

2019 ◽  
Author(s):  
Kritika Karri ◽  
David J. Waxman
Keyword(s):  
Gene Expression ◽  
Immune Response ◽  
Fatty Acid ◽  
Cell Division ◽  
Gene Regulatory Networks ◽  
Regulatory Networks ◽  
Acid Metabolism ◽  
Protein Coding ◽  
Xenobiotic Exposure ◽  
Gene Regulatory

AbstractXenobiotic exposure activates or inhibits transcription of hundreds of protein-coding genes in mammalian liver, impacting many physiological processes and inducing diverse toxicological responses. Little is known about the effects of xenobiotic exposure on long noncoding RNAs (lncRNAs), many of which play critical roles in regulating gene expression. Objective: to develop a computational framework to discover liver-expressed, xenobiotic-responsive lncRNAs (xeno-lncs) with strong functional, gene regulatory potential and elucidate the impact of xenobiotic exposure on their gene regulatory networks. We analyzed 115 liver RNA-seq data sets from male rats treated with 27 individual chemicals representing seven mechanisms of action (MOAs) to assemble the long non-coding transcriptome of xenobiotic-exposed rat liver. Ortholog analysis was combined with co-expression data and causal inference methods to infer lncRNA function and deduce gene regulatory networks, including causal effects of lncRNAs on protein-coding gene expression and biological pathways. We discovered >1,400 liver-expressed xeno-lncs, many with human and/or mouse orthologs. Xenobiotics representing different MOAs were often regulated common xeno-lnc targets: 123 xeno-lncs were dysregulated by at least 10 chemicals, and 5 xeno-lncs responded to at least 20 of the 27 chemicals investigated. 81 other xeno-lncs served as MOA-selective markers of xenobiotic exposure. Xeno-lnc–protein-coding gene co-expression regulatory network analysis identified xeno-lncs closely associated with exposure-induced perturbations of hepatic fatty acid metabolism, cell division, and immune response pathways. We also identified hub and bottleneck lncRNAs, which are expected to be key regulators of gene expression in cis or in trans. This work elucidates extensive networks of xeno-lnc–protein-coding gene interactions and provides a framework for understanding the extensive transcriptome-altering actions of diverse foreign chemicals in a key responsive mammalian tissue.

scholarly journals Persistent Cellular Immunity to SARS-CoV-2 Infection

2020 ◽  
Author(s):  
Gaëlle Breton ◽  
Pilar Mendoza ◽  
Thomas Hagglof ◽  
Thiago Y. Oliveira ◽  
Dennis Schaefer-Babajew ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Cell Division ◽  
T Cell ◽  
T Cell Responses ◽  
Memory T Cell ◽  
Cell Responses ◽  
Paired Samples ◽  
Specific Memory ◽  
Immune Alterations

AbstractSARS-CoV-2 is responsible for an ongoing pandemic that affected millions of individuals around the globe. To gain further understanding of the immune response in recovered individuals we measured T cell responses in paired samples obtained an average of 1.3 and 6.1 months after infection from 41 individuals. The data indicate that recovered individuals show persistent polyfunctional SARS-CoV-2 antigen specific memory that could contribute to rapid recall responses. In addition, recovered individuals show enduring immune alterations in relative numbers of CD4+ and CD8+ T cells, expression of activation/exhaustion markers, and cell division.SummaryWe show that SARS-CoV-2 infection elicits broadly reactive and highly functional memory T cell responses that persist 6 months after infection. In addition, recovered individuals show enduring immune alterations in CD4+ and CD8+ T cells compartments.

Cellular immune response in vitro: I. A requirement for time-dependent T-lymphocyte cell division of cytotoxic cells in the allogeneic response

1976 ◽  
Vol 8 (5) ◽  
pp. 373-381
Author(s):  
Robert L. Lundak ◽  
Marvin S. Kaplan ◽  
Donald J. Raidt ◽  
Tina S. Hronis ◽  
Gale A. Granger
Keyword(s):  
Immune Response ◽  
Cell Division ◽  
T Lymphocyte ◽  
Time Dependent ◽  
Cytotoxic Cells ◽  
Allogeneic Response ◽  
Cellular Immune ◽  
Lymphocyte Cell ◽  
Immune Response In Vitro

scholarly journals Centrosome-intrinsic mechanisms modulate centrosome integrity during fever

2015 ◽  
Vol 26 (19) ◽  
pp. 3451-3463 ◽  
Author(s):  
Anastassiia Vertii ◽  
Wendy Zimmerman ◽  
Maria Ivshina ◽  
Stephen Doxsey
Keyword(s):  
Immune Response ◽  
Heat Stress ◽  
Cell Division ◽  
Membrane Trafficking ◽  
Synapse Formation ◽  
Immunological Synapse ◽  
Formation Heat

The centrosome is critical for cell division, ciliogenesis, membrane trafficking, and immunological synapse function. The immunological synapse is part of the immune response, which is often accompanied by fever/heat stress (HS). Here we provide evidence that HS causes deconstruction of all centrosome substructures primarily through degradation by centrosome-associated proteasomes. This renders the centrosome nonfunctional. Heat-activated degradation is centrosome selective, as other nonmembranous organelles (midbody, kinetochore) and membrane-bounded organelles (mitochondria) remain largely intact. Heat-induced centrosome inactivation was rescued by targeting Hsp70 to the centrosome. In contrast, Hsp70 excluded from the centrosome via targeting to membranes failed to rescue, as did chaperone inactivation. This indicates that there is a balance between degradation and chaperone rescue at the centrosome after HS. This novel mechanism of centrosome regulation during fever contributes to immunological synapse formation. Heat-induced centrosome inactivation is a physiologically relevant event, as centrosomes in leukocytes of febrile patients are disrupted.

scholarly journals CELL-TO-CELL INTERACTION IN THE IMMUNE RESPONSE

1972 ◽  
Vol 135 (3) ◽  
pp. 711-717 ◽  
Author(s):  
R. E. Anderson ◽  
J. Sprent ◽  
J. F. A. P. Miller
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Cell Division ◽  
T Cell ◽  
Cell Interaction ◽  
Antibody Responses ◽  
Helper Function

The helper function of carrier-primed T cells was found to be radiosensitive in vivo. The results could not be attributed to interference with the spleen-seeking properties of the irradiated cells. It is suggested that T cell division is essential for the induction of 7S antibody responses in vivo.

scholarly journals THE MECHANISM OF TOLERANCE PRODUCED IN RATS TO SHEEP ERYTHROCYTES

1965 ◽  
Vol 121 (5) ◽  
pp. 683-695 ◽  
Author(s):  
Donald A. Rowley ◽  
Frank W. Fitch
Keyword(s):  
Immune Response ◽  
Cell Division ◽  
Cell Response ◽  
Sheep Erythrocyte ◽  
Passive Immunization ◽  
Small Population ◽  
Antigenic Stimulation ◽  
Sheep Erythrocytes ◽  
Growing Rats ◽  
Antibody Titers

An active immune response to sheep erythrocytes was demonstrated in rats made "tolerant" to sheep erythrocytes by twice-weekly antigen injections beginning on the day of birth. Groups of tolerant rats were sacrificed 4 days after they had received 5 to 42 antigen injections; spleens were sampled for plaque-forming (antibody-releasing) cells and sera were titrated for antibody to sheep erythrocytes using a sensitive "plate hemolysin" technique. During the 3rd week of life and after the 5th antigen injection, the tolerant rats had an immune response equivalent to that of rats of similar age which had received a single antigen injection, but spleens contained only about one-tenth as many plaque-forming cells as adults animals receiving similar antigen injections. Continued antigen injections produced a marked decline and stabilization of this relatively small population of antibody-forming cells; however, the number of plaque-forming cells in the tolerant rats remained considerably elevated above the numbers of plaque-forming cells present in the spleens of non-immunized animals. The sera from all but 1 tolerant rat had demonstrable antibody to sheep erythrocytes in low titer. A progressive recovery of the plaque-forming cell response and rise in antibody titers occurred in adult tolerant rats when the interval between the last 2 antigen injections was increased from 3 days to 14 or 28 days. The decline and stabilization of numbers of plaque-forming cells occurring with continued injections after the 3rd week of life paralleled a similar decline and stabilization in rats receiving similar antigen injections as adults. Also, the recovery of the plaque-forming cell and antibody response of tolerant animals paralleled the recovery observed when the interval between injections was increased in rats receiving similar antigen injections as adults. These findings suggested that the same mechanism controlled numbers of antibody-forming cells in tolerant and normally responsive adult animals. Repeated closely spaced antigen injections presumably interfered with either cell division or maturation of antibody-forming cells. As the interval between injections was increased, additional antibody-forming cells matured or were formed through cell division. Relatively constant antigenic stimulation provided a mechanism for controlling or limiting the response of antibody-forming cells. The mechanism controlling or limiting the response of antibody-forming cells would not account for the stabilization of numbers of antibody-forming cells at high levels for normal animals and at low levels for the tolerant animals. Passive immunization of growing rats with homologous anti-sheep erythrocyte serum markedly inhibited the plaque-forming cell response of growing rats. It was proposed that antibody produced by the small population of antibody-forming cells in the tolerant rats provided a feedback or homeostatic mechanism which inhibited transformation of potential antibody-forming cells to antibody-forming cells. Thus, tolerance to sheep erythrocytes was induced and maintained by two mechanisms. One mechanism, dependent on relatively constant antigenic stimulation, limited or controlled the numbers of antibody-forming cells. The other, dependent on the production of small quantities of antibody by a few antibody-forming cells, limited or controlled the transformation of potential antibody-forming cells to antibody-forming cells.

scholarly journals Persistent cellular immunity to SARS-CoV-2 infection

2021 ◽  
Vol 218 (4) ◽  
Author(s):  
Gaëlle Breton ◽  
Pilar Mendoza ◽  
Thomas Hägglöf ◽  
Thiago Y. Oliveira ◽  
Dennis Schaefer-Babajew ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Cell Division ◽  
T Cell ◽  
Cellular Immunity ◽  
Memory T Cells ◽  
Cell Responses ◽  
Paired Samples ◽  
Specific Memory ◽  
Cd8 Memory T Cells

SARS-CoV-2 is responsible for an ongoing pandemic that has affected millions of individuals around the globe. To gain further understanding of the immune response in recovered individuals, we measured T cell responses in paired samples obtained an average of 1.3 and 6.1 mo after infection from 41 individuals. The data indicate that recovered individuals show persistent polyfunctional SARS-CoV-2 antigen–specific memory that could contribute to rapid recall responses. Recovered individuals also show enduring alterations in relative overall numbers of CD4+ and CD8+ memory T cells, including expression of activation/exhaustion markers, and cell division.

scholarly journals THE MECHANISM OF TOLERANCE PRODUCED IN RATS TO SHEEP ERYTHROCYTES

1965 ◽  
Vol 121 (5) ◽  
pp. 671-681 ◽  
Author(s):  
Donald A. Rowley ◽  
Frank W. Fitch
Keyword(s):  
Immune Response ◽  
Cell Division ◽  
Cell Response ◽  
High Ratio ◽  
Adult Rats ◽  
Sheep Erythrocytes ◽  
Single Antigen ◽  
Antibody Titers ◽  
Marked Decline ◽  
Circulating Antibody

Previous studies suggested that an active immune response was partially responsible for maintaining immunological unresponsiveness to sheep erythrocytes. Measurement of the plaque-forming (antibody-releasing) cell response proved to be a sensitive indicator of an immune response to sheep erythrocytes in the absence of detectable circulating antibody to the antigen. The present studies were undertaken to determine whether an active immune process, measured by the plaque-forming cell response, was partially responsible for induction and maintenance of tolerance. Rats injected intraperitoneally with large doses of sheep erythrocytes beginning at the day of birth develop tolerance to the antigen. In this paper, the plaque-forming cell and antibody response to sheep erythrocytes was characterized for rats receiving a single antigen injection at various ages and for rats which received repeated antigen injections as adults. The dose of antigen was the same as that used to produce tolerance; the injection schedule for repeated immunizations was also the same as that used to produce tolerance. Rats receiving a single antigen injection on the day of birth or at age 7 days had no measurable response to the antigen. Rats receiving a single antigen injection at age 17 days and sacrificed 4 days later had an unequivocal response to the antigen. The spleens had about one-tenth as many plaque-forming cells as spleens of adult animals immunized similarly, but the antibody titers were as high as titers for adult animals. Presumably the high titers of these young animals resulted from the high ratio of plaque-forming cells to body weight and blood volume. Adult animals receiving a single antigen injection had a peak or near peak plaque-forming cell response 4 days after immunization; at this time, sera contained high titers of 19S antibody and the numbers of plaque-forming cells in spleens correlated reasonably well with circulating antibody titers. 7S antibody appeared in serum 5 or 6 days after immunization. The numbers of plaque-forming cells declined progressively 2 and 3 weeks after immunization. Repeated twice weekly, injections of the antigen in adult rats produced a marked decline and then stabilization of numbers of plaque-forming cells in spleens. Although the numbers of plaque-forming cells were fewer, titers of 19S and 7S antibody stabilized at high levels. A progressive recovery of the plaque-forming cell response and a rise in antibody titer occurred when the interval between the last 2 injections was increased from 3 to 10, 17, or 32 days. These findings suggested that repeated closely spaced antigen injections interfered with either cell division or maturation of antibody-forming cells. As the interval between injections was increased, additional antibody-forming cells matured or were formed through cell division. Thus, relatively constant antigenic stimulation provided a mechanism for controlling or limiting the response of antibody-forming cells. In the following paper, it will be shown that this mechanism operating together with a homeostatic mechanism which prevents induction of new antibody-forming cells serves to regulate the immune response to repeated injections of antigen.

scholarly journals Mechanisms of cell division as regulators of acute immune response

2014 ◽  
Vol 8 (3) ◽  
pp. 215-221 ◽  
Author(s):  
Andrey Kan ◽  
Philip D. Hodgkin
Keyword(s):  
Immune Response ◽  
Cell Division
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