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Pathogen research abs 1 || Pathogen research abs 2 || Pathogen research abs 3 || Pathogen research abs 4 || Pathogen research abs 5 || Hormone and endocrine research abs 1 || Hormone and endocrine research abs 2 || Hormone and endocrine research abs 3 || Hormone and endocrine research abs 4 || Hormone and endocrine research abs 5 || Follicle and follicular cells research abs 1 || Interferon research abs 1







Lab Invest. 1999 Feb;79(2):235-42.
Detailed in vivo analysis of interferon-gamma induced major histocompatibility complex expression in the the central nervous system: astrocytes fail to express major histocompatibility complex class I and II molecules.

Horwitz MS, Evans CF, Klier FG, Oldstone MB.

Department of Neuropharmacology, The Scripps Research Institute, La Jolla, California, USA. horwitcripps.edu

To recognize and respond immunologically to foreign antigens, T lymphocytes require the presentation of foreign peptides by MHC molecules. To determine which cells of the central nervous system (CNS) are capable of expressing MHC molecules, we used confocal microscopy and dual immunofluorescence with cell-specific and MHC-specific antibodies to study brain sections of adult mice. We took advantage of transgenic mice that initiate CNS-specific expression of IFN-gamma at 8 weeks of age. This inflammatory cytokine is a strong inducer of MHC expression both in culture and in vivo. From this analysis, we clearly found MHC class I and II expression on endothelial, microglial, and oligodendrocyte cell types, but did not find astrocytes or neurons capable of expressing either MHC class I or II molecules under these conditions. This finding suggests that, although microglia and oligodendrocytes may participate in the antigen presentation process in the organism, we found no in vivo evidence to support the concept that astrocytes act as antigen-presenting cells.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10068211&dopt=Abstract



Hepatology. 1999 Mar;29(3):897-903.
Relationship of the genomic complexity of hepatitis C virus with liver disease severity and response to interferon in patients with chronic HCV genotype 1b infection [correction of interferon]

Lopez-Labrador FX, Ampurdanes S, Gimenez-Barcons M, Guilera M, Costa J, Jimenez de Anta MT, Sanchez-Tapias JM, Rodes J, Saiz JC.

Liver Unit, Department of Medecine, Institut d'Investigacions Biomediques August Pi i Sunyer (IDIBAPS), Universitat de Barcelona, Spain.

In patients with chronic hepatitis C, the influence of the genetic heterogeneity of the hepatitis C virus (HCV) on the progression of liver disease and on the responsiveness to interferon therapy is a matter of controversy. In this study we evaluated the genetic complexity of HCV by single-strand conformation polymorphism (SSCP) analysis of amplicons from the hypervariable region 1 (HVR1) in 168 patients with chronic genotype 1b HCV infection, of whom 122 received a single course of interferon therapy (3 MU, three times weekly for 6 months). No correlation was observed between the degree of genetic complexity of HCV (indicated by the number of bands in the SSCP assay) and patient age, serum alanine aminotransferase activity, or serum HCV-RNA concentration, measured by competitive polymerase chain reaction. HCV genomic complexity was not related to gender nor to the presumed source of infection. The number of SSCP bands detected in serum samples from patients with chronic hepatitis, either mild (8.1 +/- 3.9), moderate (8.0 +/- 3.3), or severe (9.2 +/- 3.3), and in patients with liver cirrhosis, either compensated (8.0 +/- 2.9), decompensated (6.3 +/- 2.9), or with superimposed hepatocellular carcinoma (9.5 +/- 2.9), was similar. The number of SSCP bands detected in patients with sustained response (7.5 +/- 3. 9), transient response (8.3 +/- 2.9), or no response (8.2 +/- 3.6) to interferon administration was similar as well. These observations suggest that the genetic complexity of hypervariable region (HVR1) of HCV, as estimated by SSCP analysis, is not related to the severity of liver injury nor to the type of response to interferon therapy. Thus, information offered by SSCP analysis of HVR1 of HCV in chronic HCV genotype 1b infection does not appear to be useful in the clinical management of these patients. (HEPATOLOGY 1999;29:897-903.)


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10051495&dopt=Abstract



Eur J Immunol. 1999 Feb;29(2):678-85.
Differential induction of monocyte chemotactic protein-3 in mononuclear leukocytes and fibroblasts by interferon-alpha/beta and interferon-gamma reveals MCP-3 heterogeneity.

Menten P, Proost P, Struyf S, Van Coillie E, Put W, Lenaerts JP, Conings R, Jaspar JM, De Groote D, Billiau A, Opdenakker G, Van Damme J.

Rega Institute, Laboratory of Molecular Immunology, University of Leuven, Belgium.

Monocyte chemotactic protein-3 (MCP-3) is a pluripotent CC chemokine, attracting most leukocytic cell types. With the use of a sensitive and specific ELISA, MCP-3 was found to be inducible in fibroblasts and peripheral blood mononuclear cells (PBMC) by cytokines and cytokine inducers. MCP-3 production levels (1-10 ng/ml) were tenfold lower compared to those of MCP-1. In diploid fibroblasts, synergistic induction of MCP-3, but not of MCP-1, mRNA and protein was observed by combined treatment with IL-1beta and IFN-gamma. In PBMC, IFN-alpha and IFN-beta (but not IFN-gamma), as well as measles virus and double-stranded RNA, were potent inducers of MCP-3, which suggests a role for this chemokine in an early stage of viral infections. In contrast, endotoxin failed to induce MCP-3 production in fibroblasts and PBMC. Purification of MCP-3 from PBMC revealed biochemical heterogeneity. In monocyte chemotaxis and calcium mobilization assays, pure 11-kDa MCP-3 from PBMC showed similar potencies as MCP-3 from tumor cells. It was concluded that the induction of MCP-3 by IFN is regulated differently in fibroblasts and PBMC. In view of the multiple target cells for MCP-3, local and strictly regulated chemokine production might be important to conduct selectively the immune response in infection or inflammation.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10064085&dopt=Abstract



Rinsho Ketsueki. 1999 Jan;40(1):59-62.
[Rapid recovery of hemopoiesis and alleviation of symptoms similar to peri-engraftment syndrome after donor leukocyte infusion]

[Article in Japanese]

Azuma T, Hara M, Kojima K, Nawa Y.

Division of Hematology, Ehime Prefectural Central Hospital.

A 28-year-old man who had received an allogeneic bone marrow transplant 7 years earlier experienced a relapse of chronic myelogenous leukemia in an accelerated phase. He was unsuccessfully treated with vincristine (VCR) and interferon-alpha (IFN-alpha), and subsequently received a donor leukocyte transfusion (CD3+ cells: 1.5 x 10(7)/kg). Rapid hematologic recovery was observed and a complete remission was obtained without graft-versus-host disease (GVHD) or bone marrow aplasia. It may be that the preceding regimen of chemotherapy (VCR + IFN-alpha) contributed to the patient's recovery by reducing the tumor burden.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10067099&dopt=Abstract



J Infect Dis. 1999 Apr;179(4):980-8.
Interferon-gamma responses are associated with resistance to reinfection with Plasmodium falciparum in young African children.

Luty AJ, Lell B, Schmidt-Ott R, Lehman LG, Luckner D, Greve B, Matousek P, Herbich K, Schmid D, Migot-Nabias F, Deloron P, Nussenzweig RS, Kremsner PG.

Department of Parasitology, Institute for Tropical Medicine, University of Tubingen, 72074 Tubingen, Germany. adrian. lutni-tuebingen.de

The contribution of T cell-mediated responses was studied with regard to resistance to reinfection in groups of Gabonese children participating in a prospective study of severe and mild malaria due to infection with Plasmodium falciparum. In those admitted with mild malaria, but not in those with severe malaria, production of IFN-gamma by peripheral blood mononuclear cells (PBMC) in response to either liver-stage or merozoite antigen peptides was associated with significantly delayed first reinfections and with significantly lower rates of reinfection. Proliferative or tumor necrosis factor responses to the same peptides showed no such associations. Production of interferon-gamma by PBMC in response to sporozoite and merozoite antigen peptides was observed in a higher proportion of those presenting with mild malaria. Differences in the Th1/Th2 cytokine balance may be linked to the ability to control parasite multiplication in these young children, helping to explain the marked differences observed in both susceptibility to infection as well as in clinical presentation.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10068595&dopt=Abstract








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