Anti-Ata causing mild hemolytic disease of the newborn

We report here a case of moderately severe hemolytic disease of the newborn (HDN) due to anti-Ata. The gravida 5 proposita was group A rr and previously was found to have anti-Ata and -D. At the 35-week mark of this pregnancy, her anti-Ata demonstrated a titer of 256, score 79. Fluid obtained by amniocentesis at 36 weeks showed an optical density at 450 nm of 0.08 (midzone). The baby was delivered at 38 weeks by cesarean section. The cord cells were group A rr with a 3+ direct antiglobulin test. The dichloromethane eluate of the infant's cells demonstrated anti-Ata specificity only. At birth, the infant's total bilirubin (TB) was 2.1 mg per dl and the hematocrit level (Hct) was 33.8 percent. Within 8 hours, the TB had risen to 3.8 mg per dl. Phototherapy was initiated at 7-1/2 hours and maintained for 40 hours. The infant's TB rose to a maximum level of 10.5 mg per dl 24 hours after phototherapy was discontinued. At discharge 4 days postpartum, the infant's TB had dropped to 9.2 mg per dl, and the Hct value was 38 percent. On a visit 7 days postpartum, the infant's TB level had fallen to 6.5 mg per dl and the hct value was 38 percent. Transfusions were not necessary.     

Approaches to preventing or reversing platelet alloimmunization using animal models

Animal transfusion models were established to assess treatment programs for preventing or reversing platelet alloimmunization. Five control baboons given weekly transfusions of radiolabeled platelets from a single unrelated donor became immunized after an average of 2.4 +/- 2.1 transfusions. Similarly, 18 of 21 (86%) dogs given up to eight platelet transfusions from a single unrelated donor became immunized after an average of 2.3 +/- 1.7 transfusions. In six of seven baboons, prednisone or antithymocyte globulin alone or in combination effectively delayed platelet alloimmunization. In contrast, only two of 12 (17%) dogs given prednisone or antithymocyte serum (ATS) resisted alloimmunization. Neither splenectomy nor cyclophosphamide prevented alloimmunization in the baboon. In addition, attempts to reduce the immunogenicity of transfused platelets by inactivating the contaminating leukocytes with gamma radiation or by giving leukocyte-poor platelets were of no benefit in dogs. Reversal of platelet alloimmunization was achieved in two of three dogs treated with ATS and procarbazine hydrochloride. However, neither splenectomy, cyclophosphamide, ATS plus prednisone, nor vincristine sulfate produced any improvement. These studies show that the highly immunogenic nature of platelet transfusions in animals makes feasible the study of the prevention and reversal of platelet alloimmunization.     

胶原诱导性关节炎的评定与T细胞受体-热休克蛋白70DNA疫苗的保护作用

目的:纯化制备含有编码T细胞受体(TCR)Vβ5.2/8.2基因片段与结核杆菌热休克蛋白(HSP)70的一段保守序列P111-125的嵌合DNA疫苗,观察其对胶原诱导性关节炎的保护性作用。方法:实验于2006-07/2007-02在首都医科大学免疫学系实验室完成。①实验分组:36只Lewis大鼠随机分为6组,即正常对照组、胶原诱导性关节炎对照组、空质粒组、pTARGET-TCRVβ5.2-HSP70重组质粒治疗组、pTARGET-TCRVβ8.2-HSP70重组质粒治疗组及pTARGET-TCRVβ5.2-HSP70和pTARGET-TCRVβ8.2-HSP70重组质粒联合治疗组,每组6只。②实验方法:大量纯化制备重组DNA疫苗pTARGET-TCRVβ5.2-HSP70、pTARGET-TCRVβ8.2-HSP70和空质粒pTARGET,观察重组DNA疫苗对胶原诱导性关节炎的保护效果,包括关节炎指数评分、Eli-spot法测定脾细胞分泌的干扰素γ和白细胞介素4的水平、ELISA法测定血清中抗Ⅱ型胶原抗体的水平;光镜下观察大鼠后肢足关节的病理学变化。结果:36只Lewis大鼠均进入结果分析。重组DNA疫苗pTARGET-TCRVβ5.2-HSP70和pTARGET-TCRVβ8.2-HSP70对胶原诱导性关节炎有较好的保护性作用,与胶原诱导性关节炎对照组相比,关节炎指数(P<0.05)下降,炎性细胞因子干扰素γ水平(P<0.05)和抗Ⅱ型胶原抗体水平(P<0.01)降低,抑制性细胞因子白细胞介素4水平(P<0.05)升高,病理学改变较轻。且两种重组质粒联合治疗的效果要比单种质粒好。结论:重组DNA疫苗pTARGET-TCRVβ5.2-HSP70和pTARGET-TCRVβ8.2-HSP70能明显减轻胶原诱导性关节炎大鼠的关节炎症状和病理改变,二者联合应用效果更佳。     

Lack of evidence of hepatitis C infection in 290 blood component recipients, demonstrated by several single-antigen research immunoassays

BACKGROUND: A group of 290 transfusion recipients enrolled in a prospective study of posttransfusion hepatitis was studied to determine the possibility of previously unrecognized hepatitis C virus (HCV) transmission. STUDY DESIGN AND METHODS: Before and after transfusion, blood specimens that were negative in first-generation enzyme immunoassay (EIA) were tested by current commercial EIAs, several single-antigen research EIAs, and supplemental tests. RESULTS: Current second- and third-generation EIAs identified five subjects (1.7% of total) who had chronic hepatitis C before transfusion. Twenty additional sera had some reactivity with research EIAs. However, those results were the same before and after transfusion (n = 7), had reverted to partially reactive or nonreactive (n = 8), or could not be confirmed by serologic tests or polymerase chain reaction in follow-up specimens (n = 5). CONCLUSIONS: Transient or restricted reactivity to HCV antigens measured by more sensitive research EIAs does not seem to correspond to recent HCV transmission by transfusion. Whether such reactivity could reflect remote HCV infection, with the potential for chronic or intermittent viremia, remains to be determined.     

慢性胃病脾虚患者胃窦粘膜胃泌素细胞和分泌生长抑素细胞的变化及其意义

目的：观察以慢性胃病为主的脾虚患者胃窦粘膜分泌胃泌家(Gas)细胞(G细胞)、生长抑素(SS)细胞(D细胞)与脾虚证发生的关系。方法：将84例脾虚患者分为脾胃虚寒组、脾虚夹热组、胃阴不足组、脾胃湿热组、肝胃不和组，应用免疫组化技术标记胃窦粘膜G、D细胞，并定量分析。结果：以慢性胃病为主的脾虚证患者G、D细胞数均减少，D细胞面积缩小，G/D细胞数和细胞面积比值均增高(P＜0．05)。结论：G、D细胞的变化可能是慢性胃病脾虚证胃肠功能障碍的一个重要病理机制。     

Radiographic damage in large joints in early rheumatoid arthritis: relationship with radiographic damage in hands and feet, disease activity, and physical disability

An assessment of the onset of radiographic damage in the large joints (hip, knees, shoulders, elbows, ankles and tarsus) in patients with early rheumatoid arthritis, and the relationship of the progression of large joint damage with joint damage in hands and feet, with physical disability, and with cumulative disease activity, was performed in a prospective 6 yr follow-up study. Large joint damage appeared to be an early phenomenon with 20% of the patients having some damage in at least one large joint within 1 yr, and 50% of the patients within 6 yr after disease onset. Radiographic damage in large joints was significantly related to the damage in hands and feet, the physical disability index, and the cumulative disease activity. The initial disease activity at study entry was the only prognostic factor that reached significance.      

Interleukin-12 inhibits murine graft-versus-host disease

Interleukin-12 (IL-12) is a potent immunostimulatory cytokine and an inducer of type-1 T-helper cell activity and of cytotoxic T lymphocyte and natural killer cell function. We report here the paradoxical observation that a single injection of 4,900 IU of recombinant murine IL-12 inhibits acute graft-versus-host disease (GVHD) in a fully major histocompatibility complex (MHC) plus multiple minor antigen-mismatched bone marrow transplantation (BMT) model (A/J-->B10). The protective effect was enhanced by administration of T-cell-depleted host-type BM cells, and complete donor-type lymphohematopoietic reconstitution was observed in most animals. Treatment with a protective course of IL-12 led to increased serum interferon-gamma (IFN-gamma) levels as compared with those for GVHD controls at early time points, when IFN-gamma was produced predominantly by host-type natural killer cells, but led to almost complete inhibition of the later GVHD-associated increase in serum IFN-gamma levels, when IFN-gamma is produced predominantly by CD4+ T cells. Furthermore, IL-12 treatment was associated with marked alterations in the kinetics of donor T-cell expansion. Reductions in donor CD4+ and CD8+ T cells were observed in the spleen on day 4 post- BMT, but a marked increase in donor CD8+ cells was observed on day 7. Unlike broadly immunosuppressive methods for inhibiting GVHD, which are associated with loss of antileukemic effects, IL-12 has the potential to mediate antileukemic effects of its own; therefore, the GVHD- inhibitory effects of IL-12 described here suggest a potential application for this cytokine in clinical BMT.