Primary Immune Response of Mouse Spleen Cells in a Serum-Free System: the Role of 2-Mercaptoethanol

Pathobiology ◽  
1980 ◽  
Vol 48 (1) ◽  
pp. 45-50
Author(s):  
M. Burger ◽  
M.W. Hess ◽  
H. Cottier
1972 ◽  
Vol 25 (5) ◽  
pp. 345-353 ◽  
Author(s):  
MASANOBU SUGIMOTO ◽  
SHIN-ICHI TAMURA ◽  
TAKESHI KURATA ◽  
YASUYUKI EGASHIRA

2019 ◽  
Vol 20 (2) ◽  
pp. 271 ◽  
Author(s):  
Przemyslaw Zdziarski

Although the existing paradigm states that cytomegalovirus (CMV) reactivation is under the control of the cellular immune response, the role of humoral and innate counterparts are underestimated. The study analyzed the host–virus interaction i.e., CMV-immune response evolution during infection in three different clinical situations: (1) immunodeficient CMV-positive human leukocyte antigen (HLA)-matched bone marrow recipients after immunoablative conditioning as well as immunocompetent, (2) adult, and (3) infant with primary immune response. In the first situation, a fast and significant decrease of specific immunity was observed but reconstitution of marrow-derived B and natural killer (NK) cells was observed prior to thymic origin of T cells. The lowest CMV-IgG (93.2 RU/mL) was found just before CMV viremia. It is noteworthy that the sole and exclusive factor of CMV-specific immune response is a residual recipient antibody class IgG. The CMV-quantiferon increase was detected later, but in the first phase, phytohemagglutinin (PHA)-induced IFN-γ release was significantly lower than that of CMV-induced (“indeterminate” results). It corresponds with the increase of NK cells at the top of lymphocyte reconstitution and undetected CMV-specific CD8 cells using a pentamer technique. In immunocompetent adult (CMV-negative donor), the cellular and humoral immune response increased in a parallel manner, but symptoms of CMV mononucleosis persisted until the increase of specific IgG. During infancy, the decrease of the maternal CMV-IgG level to 89.08 RU/mL followed by clinical sequel, i.e., CMV replication, were described. My observations shed light on a unique host-CMV interaction and CMV-IgG role: they indicate that its significant decrease predicts CMV replication. Before primary cellular immune response development, the high level of residual CMV-IgG (about >100 R/mL) from mother or recipient prevents virus reactivation. The innate immune response and NK-dependent IFN-secretion should be further investigated.


2002 ◽  
Vol 25 (6) ◽  
pp. 946-953 ◽  
Author(s):  
Ji -Youn Youn ◽  
Hyo -Young Park ◽  
Jung -Won Lee ◽  
In -Ok Jung ◽  
Keum -Hwa Choi ◽  
...  

1970 ◽  
Vol 131 (2) ◽  
pp. 247-274 ◽  
Author(s):  
Marc Feldmann ◽  
Erwin Diener

Antibody-mediated suppression of the in vitro immune response to polymerized flagellin of Salmonella adelaide and to sheep erythrocytes was studied at the cellular level. Normal mouse spleen cells, preincubated in vitro with mixtures of antigen and antibody for short periods of time before being washed, did not respond to an optimal antigenic challenge in vitro, whereas similar cells treated with antibody alone gave a normal response. The degree of immune suppression was found to depend on the time of preincubation. Significant immune suppression could be induced in as short a time as 15 min, whereas profound suppression (90%) required the incubation of cells with mixtures of antigen and antibody for 4–6 hr. Mouse spleen cells treated similarly were also unable to respond subsequently to the antigen upon transfer to lethally irradiated hosts, as measured at both the level of the antigen-reactive cell and that of serum antibody production. These results were taken as evidence that in vitro an effect of antibody-mediated suppression occurred at the level of the immunocompetent cell. Similarities between immune tolerance and antibody-mediated suppression in vitro were described, and the significance of the findings discussed in the light of current concepts of the mechanism of antibody-mediated suppression.


1972 ◽  
Vol 136 (2) ◽  
pp. 305-317 ◽  
Author(s):  
Dov Theo Golan ◽  
Yves Borel

Exposure of normal mouse spleen cells in vitro to highly 125I-labeled dinitrophenyl (DNP)-protein carrier conjugates specifically inactivated cells able to mount an immune response to that hapten after in vivo challenge. The deletion was hapten specific and independent of the radioactive carrier to which the hapten was bound. DNP-binding cells were inactivated by radioactivity that was not part of the hapten, but was solely confined to the carrier moiety. The deletion of the anti-DNP response lasted 2–3 wk and could be specifically inhibited.


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