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.

Similarity Between Hepatic Graft-versus-host Disease and Primary Biliary Cirrhosis

Hematology ◽  
2002 ◽  
Vol 7 (5) ◽  
pp. 305-310 ◽  
Author(s):  
Takeshi Wakae ◽  
Hiroyuki Takatsuka ◽  
Yoshifumi Seto ◽  
Nobuo Iwata ◽  
Ako Mori ◽  
...  
Keyword(s):  
Primary Biliary Cirrhosis ◽  
Graft Versus Host Disease ◽  
Biliary Cirrhosis ◽  
Host Disease ◽  
Graft Versus Host

Secondary biliary cirrhosis as a consequence of graft-versus-host disease

1990 ◽  
Vol 98 (1) ◽  
pp. 223-225 ◽  
Author(s):  
Daniel J. Stechschulte ◽  
James L. Fishback ◽  
Abbas Emami ◽  
Paramjit Bhatia
Keyword(s):  
Graft Versus Host Disease ◽  
Biliary Cirrhosis ◽  
Host Disease ◽  
Graft Versus Host ◽  
Secondary Biliary Cirrhosis

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.

Graft versus Host Disease After Blood Transfusions in a Premature Infant

PEDIATRICS ◽  
1991 ◽  
Vol 87 (2) ◽  
pp. 247-250
Author(s):  
A. W. FUNKHOUSER ◽  
G. VOGELSANG ◽  
B. ZEHNBAUER ◽  
W. W. TUNNESSEN ◽  
W. E. BESCHORNER ◽  
...  
Keyword(s):  
Premature Infant ◽  
Graft Versus Host Disease ◽  
Recombinant Dna ◽  
Hla Typing ◽  
White Female ◽  
Normal Infant ◽  
Severe Combined Immune Deficiency ◽  
Host Disease ◽  
Graft Versus Host ◽  
Recombinant Dna Techniques

Transfusion-associated graft versus host disease (GVHD) has been reported primarily in adults with immunodeficiency secondary to malignancy and in children with severe combined immune deficiency, Wiskott-Aldrich syndrome or erythroblastosis fetalis after intrauterine transfusion and exchange transfusions.1-8 We have recently seen a premature, but otherwise apparently normal, infant in whom GVHD developed after simple blood transfusion. Engraftment of foreign lymphocytes from one donor was documented by HLA typing and recombinant DNA techniques leading to early treatment of the GVHD in this premature infant and making this case unique. CASE REPORT The patient was a white female, 855 g birthweight, born after 252/7 weeks' gestation to an O+, human immunodeficiency virus-negative, healthy 20-year-old woman.

Use of HLA typing in the diagnostics of graft-versus-host disease of organ transplantation

1996 ◽  
Vol 47 (1-2) ◽  
pp. 135
Author(s):  
Salmela Kaija ◽  
Turakainen Hilkka ◽  
Lautenschlager Irmeli ◽  
Koskimies Saija
Keyword(s):  
Organ Transplantation ◽  
Graft Versus Host Disease ◽  
Hla Typing ◽  
Host Disease ◽  
Graft Versus Host

scholarly journals Fatal graft-versus-host disease following blood transfusion in Hodgkin's disease documented by HLA typing

Blood ◽  
1980 ◽  
Vol 55 (5) ◽  
pp. 831-834 ◽  
Author(s):  
RE Dinsmore ◽  
DJ Straus ◽  
MS Pollack ◽  
JM Woodruff ◽  
TJ Garrett ◽  
...  
Keyword(s):  
Graft Versus Host Disease ◽  
Hodgkin's Disease ◽  
Hodgkin’S Disease ◽  
Lymph Node Biopsy ◽  
Hla Typing ◽  
Blood Products ◽  
Host Disease ◽  
Graft Versus Host ◽  
Hla Dr ◽  
Hla Phenotype

Abstract Fatal graft-versus-host disease (GVHD) developed in a patient with Hodgkin's disease treated with combined chemotherapy and radiotherapy following the transfusion of 2 U of packed red blood cells. Clinical features of the GVHD included the development of exfoliative dermatitis, progressive hepatic dysfunction, aplastic anemia, and finally progressive fatal pneumonia. GVHD was documented by skin biopsy and chimerism by HLA typing. The HLA phenotype of the patient's skin fibroblasts [A3, Bw44 (w4)/A2, B15 (w4)] was appropriate for parental haplotypes and probably represented her true HLA phenotype. Lymphocytes from the patient (peripheral blood and lymph node biopsy) were of a different HLA phenotype (A3; Bw35, w38, w4, w6; Cw4), which was inappropriate for parental HLA haplotypes but identical to the HLA phenotype of one of the blood donors. The HLA-DR typing of the patient's family and of the blood donor demonstrated that the patient and the donor probably were HLA-DR identical (DRw5/DRw6), although no B lymphocytes could be obtained from the patient for direct DR typing. We are currently irradiating all blood products administered to patients with Hodgkin's disease receiving intensive treatment. Further observations will be necessary to determine whether transfusions to other cancer patients with immunodeficiency states should be restricted to irradiated blood products.

scholarly journals Pathophysiology and Diseases of the Proximal Pathways of the Biliary System

2015 ◽  
Vol 139 (7) ◽  
pp. 858-866 ◽  
Author(s):  
Yukihiro Nakanishi ◽  
Romil Saxena
Keyword(s):  
Primary Biliary Cirrhosis ◽  
Graft Versus Host Disease ◽  
Intrahepatic Cholestasis ◽  
Sclerosing Cholangitis ◽  
Bile Ducts ◽  
Biliary Cirrhosis ◽  
Drug Induced ◽  
Progressive Familial Intrahepatic Cholestasis ◽  
Drug Induced Liver Injury ◽  
Graft Versus Host

Context Diseases of the proximal pathways of the biliary system can be divided into those that affect the interlobular bile ducts and those that affect the bile canaliculi. The former include primary biliary cirrhosis, small-duct variant of primary sclerosing cholangitis, graft-versus-host disease, and drug-induced liver injury, whereas the latter include progressive familial intrahepatic cholestasis, benign recurrent intrahepatic cholestasis, intrahepatic cholestasis of pregnancy, and drug-induced liver injury. Objective To summarize the current state of knowledge of diseases of the proximal pathways of the biliary system, with special emphasis on clinical presentation, pathological features, and differential diagnosis. Data Sources Clinicopathological information was extracted from pertinent published literature. Conclusions Care of the patient with cholestasis hinges on identifying the etiology. Diagnostic steps in cholestatic conditions comprise a thorough patient history, abdominal imaging, distinct serological studies, and liver biopsy. Primary biliary cirrhosis is characterized by distinctive serological and histological findings. The small-duct variant of primary sclerosing cholangitis is very rare and difficult to diagnose; imaging of the bile ducts is not helpful. Graft-versus-host disease is characterized by damage and loss of intrahepatic bile ducts. Drugs can cause injury variably at the level of bile canaliculus or the interlobular bile duct. Loss of bile ducts may be seen with primary biliary cirrhosis, primary sclerosing cholangitis, graft-versus-host disease, and drug-induced liver injury. Progressive familial intrahepatic cholestasis and progressive familial intrahepatic cholestasis represent 2 extreme ends of the spectrum of abnormalities in transporters responsible for bile formation. Intrahepatic cholestasis of pregnancy has a variable incidence in different parts of the world and may be due to abnormalities in transporter molecules.

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