Search Results - (Author, Cooperation:D. L. Greiner)

2015-10-03

American Association for the Advancement of Science (AAAS)

0036-8075

1095-9203

Biology

Chemistry and Pharmacology

Computer Science

Medicine

Natural Sciences in General

Physics

Animals ; Dendritic Cells/immunology/virology ; HIV Infections/*immunology ; HIV-1/*physiology ; Humans ; Leukemia Virus, Murine/*physiology ; Lymph Nodes/immunology/virology ; Lymphocytes/immunology/*virology ; Macrophages/immunology/virology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Retroviridae Infections/*immunology ; Sialic Acid Binding Ig-like Lectin 1/genetics/*physiology ; Spleen/immunology/virology ; *Virus Internalization

1744-313X

Blackwell Publishing Journal Backfiles 1879-2005

Biology

Medicine

The T cell alloantigens A.R.T.-1, A.R.T.-2, Pta, Ag-F and RT-Ly-2 were examined for linkage to albinism and the haemoglobin variant Hbb, and for cell expression similarities in the rat. The A.R.T.-1 alloantigen was not linked to either A.R.T.-2, albinism or Hbb. The A.R.T.-2 alloantigen was demonstrated to be closely associated to albinism and Hbb with a recombination frequency of approximately 3% with albinism and 1% with Hbb. The four recombinants (out of 104 animals examined) were subsequently analysed with alloantisera to Ag-F, Pta and RT-Ly-2. These alloantisera detected an antigenic system(s) which appeared to co-segregate with A.R.T.-2 in the recombinants studied Characterization of the specific T cell populations expressing each alloantigen demonstrated that removal of the cells bearing any one of the alloantigens removed all the cells expressing any of the other alloantigens. These results demonstrate that the four alloantigenic systems A.R.T.-2, Pta, Ag-F and RT-Ly-2 are located in the same genetic region of linkage group I, and appear to be expressed on the same peripheral T cell subpopulation(s) in the rat.

Electronic Resource

1432-0428

Diabetes ; BB rat ; immunology ; transfusion ; prevention ; lymphocyte ; helper/inducer subset

Springer Online Journal Archives 1860-2000

Medicine

Summary Transfusions of spleen cells are known to prevent spontaneous autoimmune diabetes in susceptible BB/W rats, while T cell-depleted transfusions are ineffective. To characterize further the protective cell(s), we transfused young diabetes prone rats with splenocytes from diabetes resistant BB/W rats that were treated in vitro to enrich them in either OX8+ (suppressor/cytotoxic) T cells or W3/25+ (helper/inducer) T cells. Diabetes subsequently occurred in 19 of 29 (66%) recipients of OX8-enriched, W3/25-depleted cells and 20 of 37 (54%) controls, but in only 7 of 30 (23%) recipients of W3/25-enriched, OX8-depleted cells (p〈0.005). Transfusion of spleen cells from diabetes resistant donor rats pretreated in vivo to deplete OX8+ cells also prevented diabetes in susceptible BB/W recipients. We conclude that transfusions of W3/25+ helper/inducer splenic T lymphocytes obtained from diabetes resistant animals prevent spontaneous diabetes in the BB/W rat.

Electronic Resource

1432-0428

BB rat ; insulitis ; insulin treatment ; RT6 ; adoptive transfer ; thyroiditis

Springer Online Journal Archives 1860-2000

Medicine

Summary Prophylactic insulin administration is known to prevent hyperglycaemia in diabetes prone BB rats and non-obese diabetic mice. This study investigated the effect of insulin treatment on the development of overt diabetes, clinically inapparent anti-islet autoreactivity, and thyroiditis in RT6-depleted diabetes resistant BB rats. Fewer than 1% of these animals develop spontaneous diabetes, but if depleted of RT6+ T cells 〉50% become hyperglycaemic. We treated 30-day-old diabetes resistant rats with anti-RT6.1 monoclonal antibody, exogenous insulin, or both. Up to 60 days of age, 16 of 20 rats given antibody alone became diabetic, compared with 1 of 20 also treated with antibody plus insulin. Up to 110 days of age, only 1 of 10 rats treated with both insulin and antibody between 30 and 60 days became diabetic. Histologic study of non-diabetic insulin plus anti-RT6 antibody treated rats revealed insulitis in 3 of 9 at 60 days old, and insulitis in 3 of 8 and thyroiditis in 6 of 7 at 110 days of age. Non-diabetic animals were also found to harbour autoreactive spleen cells that adoptively transferred diabetes. Splenocytes from 60 or 110-day-old non-diabetic donors that had been treated with insulin and antibody between 30 and 60 days of age induced diabetes in 7 of 13 and 6 of 8 adoptive recipients respectively. We conclude that insulin treatment prevents clinical diabetes in the RT6-depleted diabetes resistant BB rat, but this treatment does not prevent the development of autoreactive cell populations that cause thyroiditis and adoptively transfer diabetes.

Electronic Resource