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E H Van Elven

Publications and source records attributed to E H Van Elven.

6 recordsLinked to original sources
PubMed1989

Genetics of experimental lupus nephritis: non-H-2 factors determine susceptibility for renal involvement in murine chronic graft-versus-host disease.

Chronic graft-versus-host disease (GvHD) was induced in (C57BL/10 x DBA/2)F1 and (B10.S x DBA/2)F1 hybrids by injection of DBA/2 lymphocytes. All of the animals developed GvHD. Renal disease and proteinuria occurred in all of the (C57BL/10 x DBA/2)F1 hybrids, but only in 54% of the (B10.S x DBA/2)F1. The type of renal lesion was similar in all diseased animals of both strains, i.e., immune complex glomerulonephritis (ICGN) with deposition of antibodies and complement in glomeruli. To find out whether H-2 haplotype or other factors, such as non-H-2 linked genes, determine the susceptibility for renal involvement in GvHD, we produced (B10 x B10.S)F1 x DBA/2 mice, determined their H-2 genotype serologically, and separated them into H-2b/d and H-2s/d groups. These two groups did not differ with respect to susceptibility to renal disease in the course of GvHD, which indicates that H-2 is not the decisive genetic factor. We conclude that factors not linked with H-2 exert a major influence on susceptibility to GvHD-related renal disease in these mice.

Animals↗
PubMed1981

Capacity of genetically different T lymphocytes to induce lethal graft-versus-host disease correlates with their capacity to generate suppression but not with their capacity to generate anti-F1 killer cells. A non-H-2 locus determines the inability to induce lethal graft-versus-host disease.

When comparing, in a murine model, the kind of graft-versus-host (GVH) disease (GVHD) induced by the donor strain DBA/2 on the one hand and several H-2-congenic resistant B10 donor strains on the other, we found that strain DBA/2 was a universal nonkilling GVH donor for H-2-incompatible nonirradiated F1 hybrid recipients. In this respect, DBA/2 T cells differed from those of the H-2-identical donor strain B10.D2 as well as those of other b10 donor strains. The inability of strain DBA/2 to kill by GVH reaction was not limited to certain H-2 incompatibilities in the F1 recipients, but was nonspecific. The inability to kill is determined by a dominant locus not linked to H-2. DBA/2 T cells were also incapable of inducing the severe suppression of hematocrit values, bone marrow erythropoiesis, thymic cell proliferation, and splenic IgG production in the F1 recipients that was observed after the injection of T cell from the B10 strains. However, DBA/2 T cells, in contrast with those of the B10 donor strains, were vigorous stimulators of IgG production in H-2-incompatible F1 hybrid recipients. Surprisingly, strain DBA/2 as well as the B10 donor strains had good capacity to generate anti-F1 TK cells. Taken together, these findings raise the possibility that lethal GVHD disease is not caused, or not caused exclusively, by donor killer T cells, but by those donor T cells that directly or indirectly induce a suppression of cell proliferation in certain vital organs of the recipient.

Animals↗
PubMed1977

The absence of a human thymus lymphocyte antigen (HTLA) on bosophils and mast cells.

Basophilic granulocytes and mast cells of different species have been reported to originate from thymocytes and other lymphocytes. These observations were recently confirmed when evidence was given that thymic antigen is present on rabbit basophilic granulocytes. In the study reported here, human leukocytes were tested by the immunofluorescence technique and the immunoelectron-microscopy technique to ascertain whether a human thymus lymphocyte antigen (HTLA) could be detected on their surface. We could demonstrate the presence of HTLA on T lymphocytes but not on basophilic granulocytes, nor on mast cells in Cryostat sections of various tissues.

Adenoids↗
PubMed1977

Immune complex detection by immunofluorescence on polymorphonuclear leucocytes.

Polymorphonuclear leucocytes (PMN) from patients with systemic lupus erythematosus (SLE) were isolated from defibrinated and heparinized blood. In addition, PMN from a healthy donor were incubated with sera from SLE patients and with sera containing artificially prepared immune complexes of hepatitis B surface antigen (HBsAg) and human anti-HBsAg immunoglobulin (anti-HBs) with well defined variations of the antigen/antibody ratio. To one group of blood samples, 5 mM monoiodine acetic acid (MIAA) was added to block in vitro phagocytosis. The Pmn were examined for the presence of IgG, IgM, and HBsAg by the immunofluorescence technique. PMN from defibrinated blood of SLE patients showed in up to 80% immunoglobulin (Ig)-inclusions. However, addition of 5 mM MIAA reduced the number of Ig-containing PMN to at most 40%, which levels were equal to numbers found in specimens from heparinized blood. Addition of 5 mM MIAA to heparinized blood did not reduce the number of PMN with Ig inclusions. Normal donor PMN isolated from defibrinated, heparinized, and EDT blood showed equal amounts of Ig inclusions after incubation with SLE sera, but none when MIAA had been added. In PMN incubated with HBsAg-anti HBs immune complexes with an antigen antibody ratio between 5 and 0-2, both HBsAg and IgG could be detected. It is concluded that Ig inclusions in PMN from heparinized blood from SLE patients are due to in vivo phagocytosis, presumably of circulating immune complexes. In vitro phagocytosis of Ig from SLE sera by normal donor PMN also suggests the presence of immune complexes. Dependent on the antigen-antibody ratio, artificial HBsAg/anti-HBs immune complexes can be detected by in vitro phagocytosis by PM.

Antigen-Antibody Complex↗
PubMed1977

The absence of a human thymus lymphocyte antigen (HTLA) on basophils and mast cells.

Basophilic granulocytes and mast cells of different species have been reported to originate from thymocytes and other lymphocytes. These observations were recently confirmed when evidence was given that thymic antigen is present on rabbit basophilic granulocytes. In the study reported here, human leukocytes were tested by the immunofluorescence technique and the immunoelectron-microscopy technique to ascertain whether a human thymus lymphocyte antigen (HTLA) could be detected on their surface. We could demonstrate the presence of HTLA on T lymphocytes but not on basophilic granulocytes, nor on mast cells in Cryostat sections of various tissues.

Antibodies↗