Identification of the Type of Blood-cell Responsible for the Graft-versus-Host Reaction in Chicks

Development ◽  
1959 ◽  
Vol 7 (3) ◽  
pp. 394-408
Author(s):  
P. I. Terasaki

The injection or transplantation of certain adult chicken cells into chicken embryos is known to cause a gross enlargement of the spleen and may often have fatal consequences. The enlargement produced by transplantation of adult spleen cells on to the chorioallantois has been studied by Danchakoff (1916) and by Ebert (1951, 1954). The same effect is produced by the intravenous injection of circulating white blood-cells from adult chickens (Simonsen, 1957; Terasaki, Cannon, & Longmire, 1959). The evidence of Billingham & Brent (1957, 1959), who have studied a similar phenomenon (‘runt disease’) in mice, and of Cock & Simonsen (1958) in chicks, indicates that these effects are due to the grafted adult cells reacting immunologically against the antigens of the helpless host. This type of reaction has been called the ‘graft-versus-host’ or graft against host reaction.

2009 ◽  
Vol 31 (5) ◽  
pp. 403-409 ◽  
Author(s):  
J. Nikoskelainen ◽  
K.-O. Söderström ◽  
A. Rajamäki ◽  
L. Meurman ◽  
H. Korvenranta ◽  
...  

1973 ◽  
Vol 137 (5) ◽  
pp. 1213-1225 ◽  
Author(s):  
Jan Klein ◽  
Jong M. Park

H-2 crossovers and their parental strains were arranged into 35 combinations in which the adult donor of spleen cells differed from the newborn recipient in the whole H-2 complex, or in three, two, or one region of the complex. A Simonsen splenomegaly assay was then used to test the contribution of the individual H-2 regions to the graft-versus-host reaction (GVHR). It was shown that the strongest GVHR was associated with the Ir region. Differences in the Ir region caused significant splenomegaly in spite of the fact that no antigens detectable by conventional serological methods have thus far been associated with this region. Differences in the K and D regions showed only a borderline effect on GVHR in spite of the fact that these regions code for most, if not all, of the antigens detectable by conventional serological and transplantation methods. The K region alone caused no stronger GVHR than the D legion alone; however, K + Ir region differences led to much stronger GVHR than D region differences. The Ss-Slp region also showed only a borderline effect on GVHR. Differences in two or more H-2 regions usually caused greater splenomegaly than differences in each of the regions separately. On the basis of these findings it is concluded that the strongest GVHR is caused by genes distinct from the known histocompatibility genes of the H-2 complex. It is speculated that the GVHR genes are identical with the mixed lymphocyte reaction (MLR) and Ir genes and that the product of these genes are receptors on the surface of the thymus-derived lymphocytes (T cells).


1974 ◽  
Vol 146 (2) ◽  
pp. 333-336 ◽  
Author(s):  
A. M. Munster ◽  
P. Greenberg ◽  
S. Greenberg ◽  
A. G. Leary ◽  
G. R. Gale

1981 ◽  
Vol 31 (3) ◽  
pp. 201-204 ◽  
Author(s):  
JAMES P. OKUNEWICK ◽  
RUBY F. MEREDITH ◽  
RADMILA B. RAIKOW ◽  
BARBARA J. BROZOVICH ◽  
KATHLEEN MAGLIERE

1986 ◽  
Vol 71 (2) ◽  
pp. 189-198 ◽  
Author(s):  
E. K. Lund ◽  
M. G. Bruce ◽  
M. W. Smith ◽  
A. Ferguson

1. Graft-versus-host reaction (GvHR) was induced in neonatal mice to produce crypt hyperplasia with and without stunted villi. Lactase activity was measured along individual villi of control and GvHR mice using quantitative cytochemistry. 2. Lactase activity increased in control mice as enterocytes migrated over the lower part of the villus. This increase was followed by a period when lactase activity remained approximately constant. 3. Effects produced by GvHR on this normal profile of development included an extension of the distance on the villus over which enterocytes could continue to increase lactase activity, a reduction in the time needed for an enterocyte to express lactase activity at maximal rate, and an overall decrease in the maximal lactase activity expressed by mature enterocytes. 4. These effects have been quantified by fitting logistic curves to the experimental data. 5. Parallel biochemical analyses of intestinal homogenates showed sucrase, isomaltase, trehalase and maltase activities to increase markedly 7–8 days after the injection of parental spleen cells. 6. Attention is drawn to similarities between these results and steroid induced precocious development of intestinal function in neonatal mice.


1994 ◽  
Vol 49 (9-10) ◽  
pp. 679-683 ◽  
Author(s):  
M. Kubera ◽  
M. Bubak-Satora ◽  
V. Holan ◽  
W. Krol ◽  
A. Basta-Kaim ◽  
...  

Abstract Immunomodulation of cell-mediated immunity was studied in mice treated with either lithium chloride (LiCl), anti-CD 8 monoclonal antibody or their combination. While 6-day LiCl treatment decreased the ability of their splenocytes to induce a local graft-versus-host reaction -anti-CD 8 abolished this effect. The proliferative response of spleen cells from those three groups of mice to concanavalin A stimulation in vitro was significantly increased. The natural killer (NK) cell toxicity of the mice was decreased by over 43% after the 6-day LiCl treatment, but was ×2.5 higher then the control value after a longer 21-d treatment. These results indicate that the immunomodulatory capacity of lithium is dependent on the type of cell population studied, and on the schedule of administration.


1966 ◽  
Vol 123 (1) ◽  
pp. 103-118 ◽  
Author(s):  
William L. Elkins

The graft versus host reaction (GVHR), which results from the injection of parental strain spleen cells beneath the kidney capsule of F1 hybrid rats, is transferable during its developmental phase into F1 hybrid hosts isogeneic with the primary host, but not into secondary hosts of the parental (donor) strain. Furthermore, the GVHR propagates but rarely in secondary hybrid hosts which are allogeneic with respect to the primary hosts, but which are also genetically tolerant of donor-type cells. These findings indicate that the donor cells not only initiate the GVHR but also maintain it by virtue of immunologically specific activity. Whole-body irradiation of (LBf)F1 and (LBN)F1 hosts 24 hours prior to the injection of parental (L) spleen cells results in inhibition of the subsequent GVHR to a degree commensurate with the radiation damage sustained by the lymphoid system of the host. Furthermore, propagation of transferred GVHRs did not occur if susceptible secondary hybrid hosts had been previously irradiated. These findings indicate that radiosensitive host cells play a continuing and essential role in the pathogenesis of the invasive-destructive lesion. It is concluded that the development of this lesion depends upon the continuous interaction of the specifically reactive donor-type cells with an immunologically non-specific population of host mononuclears.


1990 ◽  
Vol 171 (2) ◽  
pp. 503-517 ◽  
Author(s):  
S C Morris ◽  
R L Cheek ◽  
P L Cohen ◽  
R A Eisenberg

A chronic graft-versus-host reaction (GVH) induced in nonautoimmune mice causes a syndrome that closely resembles SLE. In this model, donor T cells react against incompatible host Ia structures and generate excessive help, which activates a subpopulation of self-reactive B cells. We have studied whether these self-reactive B cells are activated by direct interaction with alloreactive T cells or by nonspecific bystander effects. Two types of chimeras were made: double-parental chimeras, differing at both Ia and Igh allotype [B6.C20 + bm12----(B6.C20 x bm12)F1]; and control chimeras [(B6.C20 x bm12)F1----(B6.C20 x bm12)F1]. A chronic GVH syndrome was induced in the chimeras by infusion of B6 or bm12 spleen cells. Coombs and antichromatin autoantibodies were measured using Igh allotype-specific immunoassays. The double-parental chimeras that received bm12 cells made autoantibodies principally of the Igha allotype, indicating that the bm12 T cells interacted only with the Iab-bearing host B cells. Conversely, double-parental chimeras that received B6 cells made mostly Ighb autoantibodies, indicating direct cognate interaction with the Iabm12-bearing host B cells. The control chimeras made autoantibodies of both allotypes. These results indicate that autoantibodies in chronic GVH result from direct T-B interactions and not from nonspecific T cell-derived factors.


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