HLA-DR15 (DR2) is overrepresented in myelodysplastic syndrome and aplastic anemia and predicts a response to immunosuppression in myelodysplastic syndrome

被引:199
作者
Saunthararajah, Y
Nakamura, R
Nam, JM
Robyn, J
Loberiza, F
Maciejewski, JP
Simonis, T
Molldrem, J
Young, NS
Barrett, JA
机构
[1] NIH, HLA Lab, Dept Transfus Med, Bethesda, MD 20892 USA
[2] Univ Texas, MD Anderson Canc Ctr, Houston, TX 77030 USA
[3] Univ Illinois, Chicago, IL USA
[4] NHLBI, Bethesda, MD 20892 USA
[5] Natl Canc Inst, Rockville, MD USA
[6] Int Bone Marrow Transplant Registry, Milwaukee, WI USA
关键词
D O I
10.1182/blood.V100.5.1570.h81702001570_1570_1574
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The extent and importance of auto-immune mechanisms in myelodysplastic syndrome (MDS) and the role of immunosuppression in the treatment of this disease are not well defined. We report over-representation of HLA-DR2 and its serologic split HLA-DR15 in both MDS and aplastic anemia (AA). Four clinically and ethnically defined patient groups were analyzed. The HLA-DR15 antigen frequencies among North American white MDS patients (n = 72) and AA patients (n = 59), who received immunosuppressive treatment at the National Institutes of Health (NIH), were 36% and 42%, respectively. These antigen frequencies were significantly higher than that of the control population of 240 North American white NIH blood donors typed for HLA antigens by the same molecular technique (HLADR15, 21.3%, P = .01 for MDS, P <.001 for AA). Among North American white patients reported in the International Bone Marrow Transplant Registry (IBMTR), 30% of 341 MDS patients and 33% of 364 AA patients were positive for HLA-DR2. These antigen frequencies were higher than those reported for the general North American white population (HILA-DR2, 25.3%, P = .089 for MDS, P = .01 for AA). The DR15 and DR2 frequencies were significantly increased in MDS refractory anemia (RA) (P = .036 and P = .01, respectively) but not MDS refractory anemia with excess blasts. In the NIH MDS patients, HLA-DR15 was significantly associated with a clinically relevant response to antithymocyte globulin (ATG) or cyclosporine immunosuppression (multivariate analysis, P = .008). In MDS with RA, DR15 may be useful as a guide to pathophysiology, prognosis, and treatment. (C) 2002 by The American Society of Hematology.
引用
收藏
页码:1570 / 1574
页数:5
相关论文
共 40 条
[31]  
Scheid C, 1999, BLOOD, V94, p390A
[32]   INCREASED PRODUCTION OF TUMOR-NECROSIS-FACTOR-ALPHA BY PERIPHERAL-BLOOD MONONUCLEAR-CELLS IN THE PATIENTS WITH APLASTIC-ANEMIA [J].
SHINOHARA, K ;
AYAME, H ;
TANAKA, M ;
MATSUDA, M ;
ANDO, S ;
TAJIRI, M .
AMERICAN JOURNAL OF HEMATOLOGY, 1991, 37 (02) :75-79
[33]  
SMITH MA, 1991, LEUKEMIA RES, V5, P597
[34]   T-CELL-MEDIATED INHIBITION OF ERYTHROPOIESIS IN MYELODYSPLASTIC SYNDROMES [J].
SUGAWARA, T ;
ENDO, K ;
SHISHIDO, T ;
SATO, A ;
KAMEOKA, J ;
FUKUHARA, O ;
YOSHINAGA, K ;
MIURA, A .
AMERICAN JOURNAL OF HEMATOLOGY, 1992, 41 (04) :304-305
[35]   ANTILYMPHOCYTE GLOBULIN FOR MYELODYSPLASTIC SYNDROME [J].
TICHELLI, A ;
GRATWOHL, A ;
WUERSCH, A ;
NISSEN, C ;
SPECK, B .
BRITISH JOURNAL OF HAEMATOLOGY, 1988, 68 (01) :139-140
[36]  
TOYAMA K, 1993, INT J HEMATOL, V58, P53
[37]   THE MYELODYSPLASTIC SYNDROMES - DIFFERENT EVOLUTION PATTERNS BASED ON SEQUENTIAL MORPHOLOGICAL AND CYTOGENETIC INVESTIGATIONS [J].
TRICOT, G ;
BOOGAERTS, MA ;
DEWOLFPEETERS, C ;
VANDENBERGHE, H ;
VERWILGHEN, RL .
BRITISH JOURNAL OF HAEMATOLOGY, 1985, 59 (04) :659-670
[38]  
TSUJI K, 1991, 11 INT HIST COMP WOR, V2, P807
[39]   REFRACTORY MYELODYSPLASTIC ANEMIAS WITH HYPOCELLULAR BONE-MARROW [J].
YOSHIDA, Y ;
OGUMA, S ;
UCHINO, H ;
MAEKAWA, T .
JOURNAL OF CLINICAL PATHOLOGY, 1988, 41 (07) :763-767
[40]   Mechanisms of disease - The pathophysiology of acquired aplastic anemia [J].
Young, NS ;
Maciejewski, J .
NEW ENGLAND JOURNAL OF MEDICINE, 1997, 336 (19) :1365-1372