SUMMARYThere are physiological variations in the levels of leucocytes. Among these, the circadian rhythm is very important in terms of the magnitude. Since newly identified lymphocyte subsets (i.e. extrathymic T cells) have recently been detected, a comprehensive study of the circadian rhythm was conducted. All leucocytes were found to vary in number or proportion with a circadian rhythm and were classified into two groups. One group-granulocytes, macrophages, natural killer (NK) cells, extrathymic T cells, gd T cells, and CD8 þ subset-showed an increase in the daytime (i.e. daytime rhythm). The other group-T cells, B cells, ab T cells, and CD4 þ subset-showed an increase at night. Humans are active and show sympathetic nerve dominance in the daytime. Interestingly, granulocytes and lymphocyte subsets with the daytime rhythm were found to carry a high density of adrenergic receptors. On the other hand, lymphocyte subsets with the night rhythm carried a high proportion of cholinergic receptors. Reflecting this situation, exercise prominently increased the number of cells with the daytime rhythm. These results suggest that the levels of leucocytes may be under the regulation of the autonomic nervous system.
SUMMARY
A MoAb 1–22–3 (igG3) was produced in mice immunized with rat glomeruli. A blotting study indicated the antigen molecule recognized by this MoAb has a molecular weight of about 25 kD, which is the same as that of the Thy 1.1 molecule. This MoAb is capable of inducing the morphological changes similar to those induced by anti‐thymocyte serum or the anti‐Thy 1.1 MoAb, ER4 and massive proteinuria in rats by a single i.v. injection. Proteinuria started immediately after MoAb 1–22–3 injection and peaked on day 5. Reaction products were detected by immunoelectron microscopy in vitro on the limited mesangiai cell surface facing endothelial cells and in vivo in partially lysed mesangial cells 30 min alter injection. Unlike the proteinuria‐inducing MoAb ER4, reactivity of MoAb 1–22–3 was detected neither on endothelial cells, epithelial cells, nor along the glomerular basement membrane in vivo and in vitro. There is a difference in reactivity toward guinea‐pig and rabbit materials between MoAb 1–22–3 and the commercial anti‐Thy 1.1 MoAb(OX7). The antigenic determinant of MoAb 1–22–3 is concluded to be a new epitope and only the binding of MoAb 1–22–3 to this epitope proved to lead to an abnormal increase of glomerular capillary wall permeability.
SUMMARYIrreversible mesangial changes with persistent proteinuria were induced in rats given two consecutive injections 2 weeks apart ofa MoAb 1-22-3 to rat mesiingia! celi. The characteristics ofthe resuiting lesions were investigated and compared with those of the reversible change induced by a single injection. At 24 h after the second injection, mesangioiytic changes similar to those aCtcr a single inj«:tion were evident. The accumulation of macrophage-like cells in glomeruli observed at I week after the firsl injection was not evident during lhe experimental period after the second injection. Hypercellularity with the characteristics of intrinsic mesangial cell and increased mesangial matrix were already present I week after the second injection. And mesangial sclerotic change progressed up to 6 months. Deposition of collagen type 1 and type III and accumulation of collagen fibril at the ultrastructural level were evident in rats 6 months after the second injection. Proteinuria started immediately and continued ibr more than 6 months after the second injection. The mesangial sclerotic change with persistent proteinuria described here is considered lo be a belter model for investigating the mechanism of chronic progression of human mesangial proliferative giomerulonephritis.
A 9-month-old boy presented with chronic arteritis of the aorta and its major branches. The clinical manifestations at onset of his illness were compatible with those of Kawasaki syndrome. However, the febrile period lasted for 2 months despite various immunosuppressive therapies, and the levels of C-reactive protein remain high 18 months after onset. Elevated circulating immune complexes, decreased serum complement levels, hypergammaglobulinaemia and monoclonal gammopathy were observed. Active HHV-6 infection was shown by increased serum levels of antihuman herpesvirus-6 (HHV-6) IgG and IgM antibodies, and positive HHV-6 DNA in sera, peripheral blood mononuclear cells (PBMNC) and lymph nodes. HHV-6 was actively replicating in PBMNC and lymph nodes, as shown by the detection of transcripts for the virus structural antigen. These results suggest that large vessel arteritis can be associated with HHV-6 infection.
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