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L Hao

Publications and source records attributed to L Hao.

69 records · Page 4Linked to original sources

Influence of interleukin-2 on the differentiation of macrophages.

Macrophage precursor cells, enriched in the light fraction of murine bone marrow, were cultured in vitro under the influence of CSF-1 or IL-2 or both cytokines. In the presence of CSF-1 or CSF-1 and IL-2 strong proliferation occurred, whereas in the presence of only IL-2 or medium, cells did not proliferate. Thus all proliferating cells had CSF-1 receptors and thus belonged to the macrophage lineage. IL-2 induced in these cells the formation of cytoplasmic granules and concomitantly NK-like lytic activity. Under high dosage IL-2 cells further differentiated into cells containing abundant amounts of cytoplasmic granules and exerted LAK type cytotoxicity. When IL-2 was withdrawn from the culture medium, cells could be redirected to develop the properties of typical macrophages when CSF-1 was present. Thus the composition of the cytokines surrounding macrophage precursors decides on their differentiation pathway.

Animals↗

[Distribution of 8 blood group systems in Han ethnic group of Fujian Province, China].

The distribution of 19 red cell's antigens of 8 blood group systems in Han ethnic group in Fujian province, China was investigated. The gene and haloptype frequencies were as follows: p = 0.1936, q = 0.1766, r = 0.6298; p1 = 0.1427; Dia = 0.2830; m = 0.5695, n = 0.4305, S = 0.0339, s = 0.9661, MS = 0.0200, NS = 0.0139, Ms = 0.5500, Ns = 0.4161; Fya = 0.8817; Jka = 0.4767; D = 0.9314, C = 0.7617, E = 0.2357, r' = 0.0686, R1 = 0.6352, R2 = 0.1970, R0 = 0.0605, Rz = 0.0388. Le (a +) phenotype frequency = 7.94%.

Blood Group Antigens↗

Effect of cyclosporine on immunologically mediated diabetes in nonobese diabetic mice.

Spontaneous diabetes in NOD mice has an immunologically mediated cause and is a T cell-dependent process. When diabetic NOD mice are grafted with cultured BALB/c islet tissue, the islet graft is destroyed by disease recurrence in the graft. Disease recurrence is a CD4 T cell-dependent process as determined by in vivo administration of anti-CD4 or anti-CD8 monoclonal antibody prior to the grafting of islet tissue. Cyclosporine functions in the early sequence of T cell activation by regulating the production of messenger RNA for lymphokines synthesis. Cyclosporine does not inhibit the synthesis of lymphokine once the lymphokine message is present in the cell. Thus, we might expect cyclosporine to be relatively inefficient as an agent for the regulation of disease recurrence following transplantation to actively diabetic recipients, and we would expect cyclosporine to be more effective when administered before the onset of the disease. Low-dose cyclosporine treatment can prevent development of the disease when the drug is administered before the onset of disease. Data presented here show that cyclosporine is ineffective in controlling disease recurrence in the islet graft transplanted to actively diabetic animals. Also, when we eliminate CD4 T cells from the diseased animals and graft islet tissue prior to the administration of cyclosporine, we are unable to maintain a graft with low-dose cyclosporine therapy. This result leads us to conclude that, although anti-CD4 treatment controls the expression of the disease process and allows the survival and function of the islet graft, this treatment does not return diseased animals to the prediabetic condition in which the development of diabetes can be controlled by low-dose cyclosporine therapy.

Animals↗

Macrophage precursors as natural killer cells against tumor cells and microorganisms.

Macrophage precursors cells have been isolated from spleen and liver of mice and have characterized using F4/80 antibody, their proliferative response to CSF-1 and their maturation to macrophages. These nonadherent and nonphagocytic cells exert strong killing of Yac-1 tumor cells and of various microorganisms. Transplantation of these macrophage precursors into lethally irradiated allogenic hosts restores natural killer (NK) activity within 14 days. Macrophage precursors show enhanced NK activity when activated with interleukin 2. FACS analysis of F 4/80 presorted macrophage precursors reveals about 30% of the cells coexpressing NK 1.1. and F 4/80. These data support the assumption that at least a part of the NK cell compartment is derived from the myeloid lineage.

Animals↗

Role of the L3T4+ T cell in allograft rejection.

Pancreatic islet and fetal pancreas allotransplantation has been used to examine the role of the L3T4+ T cell in allograft rejection. Tissues were grafted into recipient animals depleted of peripheral L3T4+ T cells by in vivo administration of GK1.5 (anti-L3T4) monoclonal antibody to ask the question: is there a requirement for the L3T4+ T cell in graft rejection? Data show that the requirement for the L3T4+ T cell depends on either the type of tissue transplanted or type of the antigenic disparity between donor and recipient. Data also indicate that islet allograft acceptance achieved after GK1.5 treatment of the recipient is not due to tolerance induction. We therefore conclude that the cellular requirements for allograft rejection are determined by the type of tissue transplanted and the genetic disparity between donor and recipient.

Animals↗

Autoimmune diabetes in NOD mouse is L3T4 T-lymphocyte dependent.

Cultured BALB/c islets fail to function when transplanted into diabetic nonobese diabetic (NOD) mice; such grafted tissue is rapidly destroyed by disease recurrence. The cellular requirements for this graft damage are unclear. This study was designed to investigate the role of the L3T4+ T-lymphocyte subset in disease recurrence in the NOD mouse. L3T4+ T-lymphocytes were depleted by the in vivo administration of the L3T4-specific monoclonal antibody GK1.5. This treatment reduced the level of L3T4+ T-lymphocytes from an initial 43% of the peripheral blood lymphocytes to less than 4%. L3T4 levels remained at this low level for approximately 2 wk after withdrawal of GK1.5 treatment, after which the L3T4 levels slowly began to increase in the periphery. Grafting of cultured BALB/c islet tissue into GK1.5-treated diabetic NOD mice resulted in a rapid return to normoglycemia that persisted for 2-4 wk. The gradual return to the hyperglycemic condition roughly correlated with the reappearance of L3T4+ T-lymphocytes in the peripheral circulation. From these findings we conclude that the disease process in the NOD mouse is L3T4 T-lymphocyte dependent.

Animals↗

Distribution of red cell blood group systems in Bai and Hani in China.

Two ethnic groups, Bai and Hani from Yunnan Province, South-West China, were examined for red cell blood group systems, including ABO, MNSs, Rhesus, Duffy, P, Diego, XG and Lewis. The samples, 200 for Bais and 212 for Hanis, were obtained from Jianchuan County and from Yuanjiang County respectively.

ABO Blood-Group System↗