scholarly journals ANALYSIS OF GRAFT-VERSUS-HOST DISEASE IN SYRIAN HAMSTERS

1972 ◽  
Vol 135 (3) ◽  
pp. 567-578 ◽  
Author(s):  
J. Wayne Streilein
Keyword(s):  
Graft Versus Host Disease ◽  
Lymphoid Cells ◽  
Antigenic Determinants ◽  
F1 Hybrid ◽  
Host Disease ◽  
Syrian Hamsters ◽  
Graft Versus Host ◽  
Refractory State ◽  
Lymphocyte Transfer ◽  
Additional Support

The so-called refractory state, one sequela of acute graft-versus-host disease, has been studied in adult (CB x MHA)F1 hybrid Syrian hamsters inoculated with sublethal numbers of MHA-anti-CB lymphoid cells. Intracutaneous challenge of these animals with 200 million MHA-anti-CB lymphoid cells after the acute syndrome subsided failed to evoke epidermal necrolysis, whereas a similar challenge administered to normal F1 recipients invariably resulted in lethal epidermolysis. Moreover, the gradual attrition of lymphatic tissues in these hosts and their fading capacity to display adequately immune lymphocyte transfer reactions in the skin coincided with increasing evidence of host refractoriness, suggesting a causal interrelationship. It was possible to circumvent refractoriness by challenging these animals intracutaneously with MHA-anti-CB cells if: (a) the hosts had been lethally irradiated and reconstituted with F1 hematopoietic cells, or (b) the intracutaneous inocula contained admixed F1 lymphoid cells. This evidence provides additional support for the hypothesis that in GVH disease donor lymphocytes attack primarily host lymphoid cells bearing offending homologous antigens. The GVH process can continue so long as these lymphocyte-bound antigens persist within the host, and will abate only as the aggregate host lymphatic mass is effectively destroyed (hamsters) or its antigenic determinants are masked by isoantibodies (rats, mice, man?). At this point, insufficient target tissues remain for rechallenge to incite significant recrudescence of the disease.

scholarly journals Immune responses to major histocompatibility complex homozygous lymphoid cells in murine F1 hybrid recipients: implications for transfusion-associated graft-versus-host disease

Blood ◽  
1995 ◽  
Vol 86 (8) ◽  
pp. 3090-3096 ◽  
Author(s):  
LD Fast ◽  
CR Valeri ◽  
JP Crowley
Keyword(s):  
Natural Killer Cells ◽  
Immune Responses ◽  
Natural Killer ◽  
Graft Versus Host Disease ◽  
Lymphoid Cells ◽  
Killer Cells ◽  
F1 Hybrid ◽  
Host Disease ◽  
Graft Versus Host ◽  
Donor Cells

Graft-versus-host disease (GVHD) is currently encountered after bone marrow transplantation and transfusion. GVHD associated with transfusion (TA-GVHD) in apparently immunocompetent recipients has been recently reported with increasing frequency. A consistent finding in many of these cases is that the recipient received blood from a donor homozygous for one of the recipient's HLA haplotypes. However, the observed frequency of TA-GVHD is much lower than the estimated probability of this donor/recipient combination. The potential role of recipient immune responses in controlling TA-GVHD was investigated using an analogous murine model in which GVHD is induced by the injection of parental lymphoid cells into unirradiated F1 hybrid recipients. The effect of various immune manipulations of the recipient of GVHD induction was assessed by determining the number of donor lymphoid cells required to induce GVHD responses. Whereas depletion of recipient CD4+ cells increased the number of donor cells needed to induce GVHD, depletion of recipient CD8+ and natural killer cells resulted in fewer donor cells being needed to induce a GVHD response. These studies suggest a central role for functioning recipient CD8 and natural killer cells in the down-regulation of TA-GVHD development in recipients.

scholarly journals Immune responses to major histocompatibility complex homozygous lymphoid cells in murine F1 hybrid recipients: implications for transfusion-associated graft-versus-host disease

Blood ◽  
1995 ◽  
Vol 86 (8) ◽  
pp. 3090-3096 ◽  
Author(s):  
LD Fast ◽  
CR Valeri ◽  
JP Crowley
Keyword(s):  
Natural Killer Cells ◽  
Immune Responses ◽  
Natural Killer ◽  
Graft Versus Host Disease ◽  
Lymphoid Cells ◽  
Killer Cells ◽  
F1 Hybrid ◽  
Host Disease ◽  
Graft Versus Host ◽  
Donor Cells

Abstract Graft-versus-host disease (GVHD) is currently encountered after bone marrow transplantation and transfusion. GVHD associated with transfusion (TA-GVHD) in apparently immunocompetent recipients has been recently reported with increasing frequency. A consistent finding in many of these cases is that the recipient received blood from a donor homozygous for one of the recipient's HLA haplotypes. However, the observed frequency of TA-GVHD is much lower than the estimated probability of this donor/recipient combination. The potential role of recipient immune responses in controlling TA-GVHD was investigated using an analogous murine model in which GVHD is induced by the injection of parental lymphoid cells into unirradiated F1 hybrid recipients. The effect of various immune manipulations of the recipient of GVHD induction was assessed by determining the number of donor lymphoid cells required to induce GVHD responses. Whereas depletion of recipient CD4+ cells increased the number of donor cells needed to induce GVHD, depletion of recipient CD8+ and natural killer cells resulted in fewer donor cells being needed to induce a GVHD response. These studies suggest a central role for functioning recipient CD8 and natural killer cells in the down-regulation of TA-GVHD development in recipients.

scholarly journals AN ANALYSIS OF GRAFT-VERSUS-HOST DISEASE IN SYRIAN HAMSTERS

1970 ◽  
Vol 132 (1) ◽  
pp. 181-197 ◽  
Author(s):  
J. Wayne Streilein ◽  
R. E. Billingham
Keyword(s):  
Bone Marrow ◽  
Graft Versus Host Disease ◽  
Lymphoid Cells ◽  
Transfer Reactions ◽  
F1 Hybrids ◽  
F1 Hybrid ◽  
Graft Versus Host ◽  
Immune Lymphocyte ◽  
Donor Cells ◽  
Lymphocyte Transfer

The epidermolytic syndrome that can be obtained at will in F1 hybrid hamsters by the cutaneous inoculation of adequate doses of parental strain lymphoid cells has been investigated to determine whether the cutaneous lesions are due to an autoimmune process arising from the severe, initial GVH reactions in the skin. It was amply demonstrated that inoculation of donor cells into the skin was of crucial importance to the development of epidermolysis. Parental strain lymphoid cells in similar doses delivered by any other route into normal F1 hybrids failed absolutely to incite the acute syndrome. If "immune lymphocyte transfer" reactions incited by donor cells in the host's skin were surgically removed at timed intervals after inoculation, only complete excision within 24 hr prevented the appearance of epidermolysis in F1 hybrid hosts, indicating that inoculated donor cells must remain within the confines of the skin for approximately 24 hr in order to evoke the disease, persistence for longer periods of time being unnecessary for the subsequent course of the disease. However, reconstitution experiments involving the intramuscular inoculation of suspensions containing mixtures of donor cells and host lymphoid cells, in the presence or absence of epidermal cells, unequivocally indicated that no intimate exposure of lymphoid cells to putative skin-specific antigens was essential. Similarly, the elicitation of generalized epidermolysis in F1 hybrids irradiated with 300 r and then inoculated intravenously with donor cells casts further doubt on the pathogenic importance of the skin as a source of tissue-specific antigen. The results of subsequent experiments indicated that host leukocytes, rather than parenchymal cells of the dermis or the epidermis, were important contributors of the transplantation antigenic stimulus. Moreover, a series of experiments, using (CB x MHA)F1 hybrid hosts that had been lethally irradiated and reconstituted with bone marrow cells from ALS-treated MHA donors, indicated that from 6 to 10 wk after reconstitution—when direct and immune lymphocyte transfer reactions showed a virtual absence of native F1 leukocytes from the circulation—donor cells obtained from specifically sensitized MHA donors were completely ineffective in inducing epidermolysis, while equivalent lymphoid cell inocula derived from CB donors evoked the cutaneous disease irrespective of the time elapsed since reconstitution. To explain these findings it is postulated that in hamsters, the primary targets in graft-versus-host disease incited by the intracutaneous inoculation of donor cells are leukocytes originating in bone marrow or lymph node, or both.

Different strains of donor parental lymphoid cells induce different models of chronic graft-versus-host disease in murine (Balb/c × A/J)F1 hybrid hosts

1990 ◽  
Vol 56 (3) ◽  
pp. 298-310 ◽  
Author(s):  
Carmen Gelpi ◽  
M.Angeles Martinez ◽  
Silvia Vidal ◽  
Ana Algueró ◽  
Cándido Juarez ◽  
...  
Keyword(s):  
Graft Versus Host Disease ◽  
Lymphoid Cells ◽  
F1 Hybrid ◽  
Host Disease ◽  
Graft Versus Host ◽  
Different Strains

scholarly journals Type 2 innate lymphoid cells treat and prevent acute gastrointestinal graft-versus-host disease

2017 ◽  
Vol 127 (5) ◽  
pp. 1813-1825 ◽  
Author(s):  
Danny W. Bruce ◽  
Heather E. Stefanski ◽  
Benjamin G. Vincent ◽  
Trisha A. Dant ◽  
Shannon Reisdorf ◽  
...  
Keyword(s):  
Graft Versus Host Disease ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Host Disease ◽  
Graft Versus Host

Relationship between Primary Biliary Cirrhosis and Chronic Graft versus Host Disease: Investigation of Histocompatibility (HLA) Antigenic Determinants in Biliary Tract Antigens

1983 ◽  
Vol 64 (1) ◽  
pp. 113-116 ◽  
Author(s):  
I. G. McFarlane ◽  
B. M. McFarlane ◽  
A. J. Haines ◽  
A. L. W. F. Eddleston ◽  
Roger Williams
Keyword(s):  
Primary Biliary Cirrhosis ◽  
Guinea Pig ◽  
Biliary Tract ◽  
Graft Versus Host Disease ◽  
Hla Typing ◽  
Antigenic Determinants ◽  
Biliary Cirrhosis ◽  
Host Disease ◽  
Graft Versus Host ◽  
Hla System

1. According to a recent hypothesis, based on similarities between chronic graft versus host disease and primary biliary cirrhosis (PBC), immune reactions against histocompatibility (HLA) antigens-6-be responsible for the bile duct damage and extrahepatic lesions of PBC. 2. Previous studies have demonstrated autoimmune reactions in PBC against normal human biliary tract antigens. To equate these findings with the above hypothesis, it has been suggested that the biliary antigens are related to the HLA system and, in the present study, this possibility has been investigated by: (a) using preparations of the biliary antigens to inhibit the lymphocytotoxic activity of standard HLA-typing sera against normal lymphocytes, and (b) employing guinea-pig antisera raised against the biliary antigens as ‘typing reagents’ in the lymphocytotoxicity test to determine whether these antisera recognize HLA components on the surfaces of normal lymphocytes. 3. No inhibition by the biliary antigens of the reaction of two standard typing sera against T-and B-lymphocytes from two normal healthy donors (covering nine HLA-A, -B, -C and three HLA-DR loci antigens) was observed. Conversely, the guinea-pig antisera showed no reaction against these lymphocytes. 4. The results suggest that the biliary tract antigens are probably not related to ‘common’ antigenic determinants associated with the HLA system.

scholarly journals The role of interferon-gamma, nitric oxide and lipopolysaccharide in intestinal graft-versus-host disease developing in F1-hybrid mice

Immunology ◽  
2003 ◽  
Vol 109 (3) ◽  
pp. 440-449 ◽  
Author(s):  
Cynthia A. Ellison ◽  
Shannon A. Natuik ◽  
Alan R. Mcintosh ◽  
Sheila A. Scully ◽  
Dimitry M. Danilenko ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Interferon Gamma ◽  
Graft Versus Host Disease ◽  
F1 Hybrid ◽  
Host Disease ◽  
Graft Versus Host ◽  
Hybrid Mice
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