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Acta Neuropathol (Berl). 2002 Nov;104(5):513-24. Epub 2002 Jul 12.
Adoptive transfer-experimental allergic neuritis in newborn Lewis rats results in inflammatory infiltrates, mast cell activation, and increased Ia expression with only minor nerve fiber degeneration.
Pilartz M, Jess T, Indefrei D, Schroder JM.
Institut fur Neuropathologie, Universitatsklinikum der Rheinisch-Westfalischen Technischen Hochschule Aachen, Pauwelsstrasse 30, 52074 Aachen, Germany.
Experimental allergic neuritis (EAN) induced in the Lewis rat by the adoptive transfer of a P2-specific T cell line (AT-EAN) is considered an animal model of Guillain-Barre syndrome. It is not yet known whether AT-EAN is inducible at early stages in the development of the peripheral nervous system (PNS) or whether disease activity is modified because of immaturity of either the nervous system or the immune system. We therefore compared the susceptibility of neo-natal and adult Lewis rats to AT-EAN induced by the adoptive transfer (intraperitoneally) of 10(6) activated P2-specific T cells. P2 antigen was already present in 7 day old Lewis rats and P2-specific T cell transfer into 3-day-old rats induced clinical disease associated with an inflammatory response (sciatic nerves and spinal ganglia). In injected newborn rats we observed local activation of mast cells, infiltration of the PNS by inflammatory cells, and induction of Ia antigen expression in Schwann cells. Unlike in adults, segmental or paranodal demyelination despite occasional nerve fiber degeneration did not occur. However, the difference between newborn and adult rats could not be ascertained statistically because of the relative rarity of the lesions, their focal character, the admixture of fiber demyelination and degeneration, and most importantly, size differences of the myelinated fibers, which result in a large developmental decrease in fiber density in adults compared to newborns.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12410399&dopt=Abstract
Clin Infect Dis. 2002 Nov 15;35(10):1250-7. Epub 2002 Oct 28.
Fatal immune restoration disease in human immunodeficiency virus type 1-infected patients with progressive multifocal leukoencephalopathy: impact of antiretroviral therapy-associated immune reconstitution.
Safdar A, Rubocki RJ, Horvath JA, Narayan KK, Waldron RL.
Division of Infectious Diseases, Department of Medicine, University of South Carolina School of Medicine and Palmetto-Richland Memorial Hospital, Columbia, South Carolina 29203, USA. safdaichmed.medpark.sc.edu
Immune reconstitution resulting from use of highly active antiretroviral therapy in patients infected with human immunodeficiency virus type 1 (HIV-1) has been associated with a significant decrease in infectious morbidity and with improved survival. Occasionally, patients with quiescent disease due to human cytomegalovirus or nontuberculous mycobacteria may experience paradoxical worsening due to "dysregulated" restitution of the immune system (that is, immune restoration disease [IRD]). Acquired immunodeficiency syndrome-related progressive multifocal leukoencephalopathy (PML) is uncommon and often improves with immune recovery. We describe 2 HIV-1-infected patients with PML that presented with paradoxical worsening after the patients had commenced active antiretroviral therapy. After they had a transient response to high-dose corticosteroid therapy, both patients died of progressive neurological deterioration. IRD in these patients with PML was unexpected and occurred soon after they had started receiving active antiretroviral therapy, during the period of improved antigen-specific T-helper cell function. Predictors of patients' proclivity for these adverse events are uncertain. Evaluation of targeted immunomodulatory therapy directed towards disease-specific IRD is critical and may play an important role in improved survival for patients who are at risk.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12410486&dopt=Abstract
Scand J Immunol. 2002 Nov;56(5):456-69.
Subcellular redistribution and surface exposure of the Ro52, Ro60 and La48 autoantigens during apoptosis in human ductal epithelial cells: a possible mechanism in the pathogenesis of Sjogren's syndrome.
Ohlsson M, Jonsson R, Brokstad KA.
The Broegelmann Research Laboratory, Department of Microbiology and Immunology, The Gade Institute, University of Bergen, Bergen, Norway.
The Ro52, Ro60 and La48 autoantigens are associated with Sjogren's syndrome (SS) and systemic lupus erythematosus (SLE). The mechanisms behind tolerance breakdown of these self-peptides remain unclear; however, apoptosis has been proposed to cause their presentation to the immune system. We have examined the localization of transiently expressed enhanced green fluorescent protein (EGFP)-tagged Ro52, Ro60 and La48 autoantigens in a human salivary gland (HSG) cell line by laser confocal microscopy under normal growth conditions and during apoptosis. Surface exposure of Ro52, Ro60 and La48 was demonstrated on nonfixed apoptotic cells with monoclonal antibodies (MoAbs) or with primary SS patient antisera. Laser scanning cytometry determined the apoptotic frequency. EGFP alone was studied as control. We found that Ro52 mainly is cytoplasmic, Ro60 both nuclear and cytoplasmic, while La48 only resides in the nucleus under normal conditions. During early apoptosis, La48 is dramatically redistributed to the cytoplasm, while the localization of Ro52 and Ro60 is maintained. All three autoantigens filled apoptotic blebs and covered TUNEL (terminal-deoxynucleotidyl-transferase-mediated dUTP-digoxigenin nick end labelling)-positive apoptotic bodies. Identical results were obtained in COS-7 cells. We have developed a transfection system to study the intracellular localization of the three autoantigens Ro52, Ro60 and La48, without antibody detection. During apoptosis, there is an intracellular redistribution of endogenous and EGFP-tagged Ro52, Ro60 and La48, leading to surface exposure. These findings may indicate a role for apoptosis in the induction and facilitation of humoral responses to Ro52, Ro60 and La48 in the autoimmune exocrinopathy of SS.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12410795&dopt=Abstract
Science. 2002 Nov 1;298(5595):1025-9.
Toll-like receptor 4-dependent activation of dendritic cells by beta-defensin 2.
Biragyn A, Ruffini PA, Leifer CA, Klyushnenkova E, Shakhov A, Chertov O, Shirakawa AK, Farber JM, Segal DM, Oppenheim JJ, Kwak LW.
Experimental Transplantation and Immunology Branch, National Cancer Institute, Bethesda, MD 20892, USA. aryail.ncifcrf.gov
beta-Defensins are small antimicrobial peptides of the innate immune system produced in response to microbial infection of mucosal tissue and skin. We demonstrate that murine beta-defensin 2 (mDF2beta) acts directly on immature dendritic cells as an endogenous ligand for Toll-like receptor 4 (TLR-4), inducing up-regulation of costimulatory molecules and dendritic cell maturation. These events, in turn, trigger robust, type 1 polarized adaptive immune responses in vivo, suggesting that mDF2beta may play an important role in immunosurveillance against pathogens and, possibly, self antigens or tumor antigens.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12411706&dopt=Abstract
J Neural Transm. 2002 Dec;109(12):1445-52.
Moderate hyperhomocysteinaemia and immune activation in Parkinson's disease.
Widner B, Leblhuber F, Frick B, Laich A, Artner-Dworzak E, Fuchs D.
Institute of Medical Chemistry and Biochemistry, University of Innsbruck, Fritz Pregl Strasse 3, A-6020 Innsbruck, Austria.
Moderate hyperhomocysteinaemia has been linked to an increased risk for cardiovascular diseases. Increased homocysteine concentrations may follow folate depletion due to insufficient dietary intake of the vitamin, but there is also some indication that immune activation could play a role. In this preliminary study, homocysteine, folate, and vitamin B(12) concentrations were measured in 19 patients with Parkinson's disease, 61-90 years of age, and compared to a healthy control group of similar age and to neopterin concentrations as an indicator of immune activation. A subgroup of patients presented with increased homocysteine and low folate concentrations. Homocysteine levels correlated inversely with vitamins folate and B(12) and positively with neopterin concentrations. Disturbed homocysteine metabolism in Parkinson's disease may be associated with vitamin deficiency and with immune system activation which may underlie folate depletion.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12486485&dopt=Abstract
The average human scalp is covered by approximatey 100,000 hair follicles. Each hair undergoes
Loss of hair itself does not pose critical health problems because biological role of human hair is relatively marginal. Hair on our scalp protects the head from mechanical shock, heat loss, and exposure to UV-light. The eyelashes and eyebrowes protect the eyes, and hair in the ear canal or the nasal passages help filter out particles and pathogens, thus protecting our internal organs.
However, hair does play important social role: it is one of the major determinants of our appearance and identity in daily life. Fullness of hair also implicates or manifests physical integrity and youthfulness of the person. Losing hair could have more than just emotional impacts on individuals.
The hair is a unique organ that goes through a characteristic cycle consisting of an immature phase, a growing phase called anagen, a transitional phase between the growing phase and the resting phase called catagen, and finally a resting phase called telogen in which the hair stops growing, waiting to fall out. 85-90% of hairs on our body are in anagen phase or growing phase, which lasts anywhere from two to five years. This phase is followed by a short regression phase, or catagen, which lasts 2-3 weeks. Approximately 1% of hair follicles are in catagen. Approximately 10-15% of hair follicles are in the resting phase, the telogen, which lasts about 3-5 months. Hair follicles typically goes through 10-20 asynchronous cycles during the lifetime.
Persistent loss of more than 150 hairs would consist a state of hair loss, or alopecia, albeit it could be temporary.
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