Search Results - (Author, Cooperation:M. B. Oldstone)

2013-04-13

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 ; Antibodies, Viral/blood ; Antigens, CD274/metabolism ; Arenaviridae Infections/*immunology/pathology/*virology ; CD4-Positive T-Lymphocytes/immunology ; Cytokines/metabolism ; Dendritic Cells/immunology/virology ; Female ; Immune Tolerance ; Interferon Type I/immunology/*metabolism ; Interleukin-10/metabolism ; Lymphocytes/immunology/virology ; Lymphocytic choriomeningitis virus/*immunology/*physiology ; Male ; Mice ; Mice, Inbred C57BL ; Receptor, Interferon alpha-beta/immunology/metabolism ; *Signal Transduction ; Spleen/immunology/pathology ; Viremia

1365-3083

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

An association has been found between the Epstein-Barr virus (EBV) and complement (C3d) receptors on human lymphoid cells. The evidence was fourfold: there was a correlation between the expression of these two receptors; inhibition experiments showed that the binding sites probably are close to each other in the cell membrane, although not identical; EBV and complement receptors have been found to co-cap in either order; and lymphoid cell lines lacking complement receptors could not be superinfected with EBV.

Electronic Resource

1365-3083

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Electronic Resource

1432-2307

Type 2 (non-insulin-dependent) diabetes mellitus ; Human cytomegalovirus ; Major histocompatibility complex II ; Islet amyloid polypeptide

Springer Online Journal Archives 1860-2000

Medicine

Summary Human cytomegalovirus (HCMV) was recently demonstrated in the pancreas of about half the patients with type 2 diabetes mellitus in the absence of mumps, rubella or Coxsackie B virus. The present study addresses the question as to whether type 2 diabetes with an HCMV-positive pancreas differs from those with HCMV-negative pancreases with respect to age, sex, treatment, duration of disease, volume densities of B-cells and D-cells, mRNA levels of insulin and somatostatin, islet amyloid peptide deposits and major histocompatibility complex (MHC) class I and class II gene transcription, and protein expression. HCMV-positive type 2 diabetic patients showed a tendency towards a shorter duration of disease and significantly increased levels of MHC class II on RNA. In addition, expression of MHC class II product (HLA-DR) was identified in duct epithelial cells and/or islet cells in 9 diabetic pancreases and in 2 non-diabetic glands. No MHC class I expression could be detected. No other clinical differences between HCMV-positive and HCMV-negative glands were found. All 10 HCMV-positive diabetics showed a strong expression of MHC class II mRN in the pancreas. By immunocytochemistry, 4 of 10 demonstrated expression on the islets; three of ten also expressed MHC DRβ on ductal cells. This finding might be related to the viral infection, as only 2 of the 9 HCMV-negative patients were HLA-DRβ positive and none of the non-diabetic controls showed increased levels of MHC class II mRNA. These data suggest that HCMV infection in the pancreas is associated with type 2 diabetes. However, no conclusions as to a role of this virus in the aetiopathology of type 2 diabetes can be drawn at present.

Electronic Resource

1432-0533

Key words Reactive astrocytes ; Central nervous ; system ; Immunocytochemistry

Springer Online Journal Archives 1860-2000

Medicine

Abstract Astrocytes respond vigorously to diverse neurological insults. It is still not clear, however, whether this response is stereotypic following different insults or varies according to the injury. We have used a novel immunocytochemical marker of reactive astrocytes, termed M22, together with antibodies to glial fibrillary acidic protein (GFAP), to analyze region- and insult-specific differences in reactive astrocytosis in the murine central nervous system (CNS). Pathology was variously induced by (1) infectious agents, (2) transgenic overexpression of a viral glycoprotein or cytokine, or (3) focal trauma. Scrapie infection induced high levels of both GFAP and M22 epitope expression by hippocampal reactive astrocytes, but neither scrapie nor wild mouse retrovirus infection induced detectable M22 staining in reactive astrocytes of the caudal brain. Focal trauma and human immunodeficiency virus gp120 overexpression induced M22 expression only in the hippocampus, while interleukin-6 overexpression induced it in cerebellar astrocytes. Although M22 expression was limited to areas with extensive damage, GFAP expression was induced in every region of the mouse brain displaying pathology. Staining of routinely fixed human brain tissue demonstrated that M22 also labeled reactive astrocytes in chronic human CNS disease. The restriction of M22 expression to areas of strongly GFAP-positive astrocytosis suggests that the M22 antibody identified highly activated reactive astrocytes. Because of this selective staining of activated astrocytes, the M22 antibody may provide neuropathologists with a good marker for qualitative analysis of the astrocytic response to different injuries.

Electronic Resource

1420-9071

Key words. Immunology; immunosuppression; virus; infection.

Springer Online Journal Archives 1860-2000

Biology

Medicine

Abstract. Following infection, a virus must battle against the host's immune response. Viruses have developed many ways to escape immune surveillance and downregulate the host’s immune response. Some viruses cause a generalized immunosuppression, thereby inhibiting or depressing the immune response towards themselves as well as towards unrelated pathogens. This review will focus on the mechanisms involved in the three main human viral infections causing immunosuppression: measles, human immunodeficiency virus and cytomegalovirus. We will also discuss what has been learned from the extensively studied mouse models of viral-induced immunosuppression: lymphocytic choriomeningitis virus and Rauscher Leukemia Virus. All of these viruses that induce generalized immunosuppression appear to do so by very similar mechanisms. They hinder antigen presentation to T cells and/or hematopoiesis. We will highlight the similarities in the viral targets as well as present evidence for alternate mechanisms.

Electronic Resource

1432-1831

Springer Online Journal Archives 1860-2000

Medicine

Abstract Human peripheral blood lymphocytes (PBL) harvested after vaccination with vaccinia or measles virus showed a specific activity against virusinfected target cells. This activity peaked on day 7 and was specific for the target cells infected with the virus used for the vaccination. The cytotoxic activity was not related to HLA markers. The cells involved in the cytolytic process were lymphocytes bearing Fc receptors. In addition, the cytotoxic activity was abrogated by more than 90% by rabbit Fab'2 anti-human IgG. It is therefore likely that two subpopulations of lymphocytes are involved: an antibody-secreting cell providing specific antiviral antibody and an effector cell bearing Fc receptor (K cells). Finally, these experiments suggest that antibody-dependent cell cytotoxicity may play a major role in the recovery from virus infection in man.

Electronic Resource

1432-1831

Springer Online Journal Archives 1860-2000

Medicine

Electronic Resource

1432-1831

Springer Online Journal Archives 1860-2000

Medicine

Electronic Resource

1432-1831

Springer Online Journal Archives 1860-2000

Medicine

Electronic Resource

1432-1831

Springer Online Journal Archives 1860-2000

Medicine

Electronic Resource

1432-1831

Springer Online Journal Archives 1860-2000

Medicine

Electronic Resource

1432-1831

Springer Online Journal Archives 1860-2000

Medicine

Electronic Resource