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189 records – page 1 of 19.

Activation of the immune system and systemic immune-complex deposits in Brown Norway rats with dental amalgam restorations.

https://arctichealth.org/en/permalink/ahliterature72544
Source
J Dent Res. 1998 Jun;77(6):1415-25
Publication Type
Article
Date
Jun-1998
Author
P. Hultman
U. Lindh
P. Hörsted-Bindslev
Author Affiliation
Department of Health and Environment, Linköping University, Sweden.
Source
J Dent Res. 1998 Jun;77(6):1415-25
Date
Jun-1998
Language
English
Publication Type
Article
Keywords
Analysis of Variance
Animals
Antibody Formation - drug effects
Antigen-Antibody Complex - analysis - blood
Autoimmune Diseases - chemically induced
Autoimmunity
Body Burden
Comparative Study
Copper - analysis
Dental Amalgam - toxicity
Dinitrobenzenes
Female
Immune Complex Diseases - chemically induced
Immunoglobulin E - blood
Laminin
Lymphocyte Activation - drug effects
Mercury - analysis - blood - pharmacokinetics
Rats
Rats, Inbred BN
Rats, Inbred Lew
Research Support, Non-U.S. Gov't
Silver - analysis
Spectrum Analysis, Mass
Statistics, nonparametric
Tissue Distribution
Abstract
Dental amalgam restorations are a significant source of mercury exposure in the human population, but their potential to cause systemic health effects is highly disputed. We examined effects on the immune system by giving genetically mercury-susceptible Brown Norway (BN) rats and mercury-resistant Lewis (LE) rats silver amalgam restorations in 4 molars of the upper jaw, causing a body burden similar to that described in human amalgam-bearers (from 250 to 375 mg amalgam/kg body weight). BN rats with amalgam restorations, compared with control rats given composite resinous restorations, developed a rapid activation of the immune system, with a maximum 12-fold increase of the plasma IgE concentration after 3 wks (p 0.05). After 12 wks, BN rats with amalgam restorations showed significantly increased (p spleen > cerebrum occipital lobe > cerebellum > liver > thymus, and the tissue silver concentration was significantly (p
PubMed ID
9649170 View in PubMed
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Adoptive transfer of experimental autoimmune uveoretinitis in HgCl2 injected rats.

https://arctichealth.org/en/permalink/ahliterature57752
Source
Curr Eye Res. 1992;11 Suppl:101-5
Publication Type
Article
Date
1992
Author
A. Saoudi
B. Bellon
Y. de Kozak
P. Druet
Author Affiliation
Pathologie rénale et vasculaire, INSERM U28, Hôpital Broussais, Paris, France.
Source
Curr Eye Res. 1992;11 Suppl:101-5
Date
1992
Language
English
Publication Type
Article
Keywords
Animals
Antigens - immunology
Arrestin
Autoantigens - immunology
Autoimmune Diseases - immunology - therapy
Disease Models, Animal
Eye Proteins - immunology
Female
Immunoglobulin E - analysis
Immunotherapy, Adoptive
Male
Mercuric Chloride
Rats
Rats, Inbred BN
Rats, Inbred Lew
Research Support, Non-U.S. Gov't
Retinitis - immunology - therapy
T-Lymphocytes - immunology
Uveitis - immunology - therapy
Abstract
We previously demonstrated that mercuric chloride (HgCl2) injected-(Lewis x Brown-Norway) F1 rats are protected against experimental autoimmune uveoretinitis (EAU) induced by active immunization with the retinal S-antigen (S-Ag). To better understand the mechanisms of the protection promoted by HgCl2, we studied the effect of HgCl2-induced autoimmune disease on transferred EAU. We demonstrate herein that HgCl2 has no effect on adoptively transferred EAU. Therefore, the HgCl2-induced autoimmune disease does not affect effector S-Ag specific T cells activated in vitro but acts at an earlier stage.
PubMed ID
1424735 View in PubMed
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Age-related changes in noradrenergic sympathetic innervation of the rat spleen is strain dependent.

https://arctichealth.org/en/permalink/ahliterature9978
Source
Brain Behav Immun. 2002 Jun;16(3):247-61
Publication Type
Article
Date
Jun-2002
Author
Denise Bellinger
Lily Tran
Joey I Kang
Cheri Lubahn
David L Felten
Dianne Lorton
Author Affiliation
Center for Neuroimmunology, Loma Linda University School of Medicine, 11021 Campus Street, Loma Linda, CA 92352, USA.
Source
Brain Behav Immun. 2002 Jun;16(3):247-61
Date
Jun-2002
Language
English
Publication Type
Article
Keywords
Aging - physiology
Animals
Arterioles - innervation
Comparative Study
Male
Neuroimmunomodulation - physiology
Norepinephrine - analysis
Rats
Rats, Inbred BN
Rats, Inbred F344
Rats, Inbred Lew
Research Support, U.S. Gov't, P.H.S.
Species Specificity
Spleen - blood supply - chemistry - innervation
Sympathetic Nervous System - chemistry - physiology
Abstract
Previous findings from our laboratory revealed an age-related decline in noradrenergic (NA) sympathetic innervation of the spleen in male Fischer 344 (F344) rats. The purpose of this study was to determine whether other rat strains also progressively lose NA sympathetic nerves in the aging spleen. Sympathetic innervation of spleens from 3- and 21-month-old male F344, Brown Norway (BN), BN X F344 (BNF(1)), and Lewis rats was examined using fluorescence histochemistry to localize catecholamines combined with morphometric analysis and using high-performance liquid chromatography with electrochemical detection for measuring norepinephrine (NE). Neurochemistry revealed a significant age-related decline in NE concentrations in spleens from F344 and Lewis rats. In contrast, there was no effect of age on splenic NE concentrations in BN or BNF(1) rats. Consistent with neurochemical analysis, fluorescence histochemistry revealed a striking decline in NA innervation of spleens from old F344 and Lewis rats not observed in the other two strains. However, in BN and BNF(1) rats, nerve fibers were diminished in distal portions of the spleen but not in the hilar regions. Morphometric analysis confirmed neurochemical and histological findings, revealing approximately 65-70% loss in NA nerve density in spleens from F344 and Lewis rats. These findings indicate that age-related changes in sympathetic innervation of the rat spleen are strain-dependent. Whether the loss of sympathetic nerves in spleens from F344 and Lewis rats is associated with age-related changes in the splenic microenvironment remains to be determined. The functional significance of altered sympathetic innervation of the spleen with advancing age is discussed.
PubMed ID
12009685 View in PubMed
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Age-related susceptibility to experimental autoimmune myasthenia gravis: immunological and electrophysiological aspects.

https://arctichealth.org/en/permalink/ahliterature57596
Source
Muscle Nerve. 1997 Sep;20(9):1091-101
Publication Type
Article
Date
Sep-1997
Author
A C Hoedemaekers
J J Verschuuren
F. Spaans
Y F Graus
S. Riemersma
P J van Breda Vriesman
M H De Baets
Author Affiliation
Department of Immunology, Maastricht University, The Netherlands.
Source
Muscle Nerve. 1997 Sep;20(9):1091-101
Date
Sep-1997
Language
English
Publication Type
Article
Keywords
Aging - immunology - physiology
Animals
Antibodies - immunology
Chronic Disease
Disease Susceptibility
Electrophysiology
Female
Immunization
Myasthenia Gravis - immunology - physiopathology
Neuromuscular Junction - physiopathology
Osmolar Concentration
Rats
Rats, Inbred BN
Rats, Inbred Lew
Receptors, Cholinergic - immunology - metabolism
Research Support, Non-U.S. Gov't
Synaptic Transmission
Abstract
Susceptibility to experimental autoimmune myasthenia gravis (EAMG) was found to decrease with aging in both Lewis and Brown Norway (BN) rats. In this study, the difference in susceptibility between young and aged Lewis and BN rats was used to analyze factors determining the clinical severity of EAMG. The incidence and severity of muscular weakness did not correlate with acetylcholine receptor (AChR) loss nor with the ability of antibodies to interfere with AChR function. Aged rats showed significantly lower anti-rat AChR antibody titers than young rats and developed less severe or no clinical signs of disease. In individual young or aged rats, however, no significant correlation was found between the clinical signs of disease and anti-rat AChR titer. Neuromuscular transmission was found to change with aging as measured by single-fiber electromyography (SFEMG). In aged BN rats, increased jitter and blockings were found even before EAMG induction. Despite this disturbed neuromuscular transmission, these aged BN rats were clinically resistant against induction of EAMG. The results of this study indicate that the age-related susceptibility to EAMG is influenced by factors determined by the immune attack as well as mechanisms at the level of the neuromuscular junction.
PubMed ID
9270663 View in PubMed
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The alloantibody response and active enhancement of some rat renal allografts.

https://arctichealth.org/en/permalink/ahliterature57941
Source
Transplantation. 1977 Mar;23(3):230-8
Publication Type
Article
Date
Mar-1977
Author
S B Desi
M. Ruszkiewicz
Source
Transplantation. 1977 Mar;23(3):230-8
Date
Mar-1977
Language
English
Publication Type
Article
Keywords
Animals
Bone Marrow - immunology
Bone Marrow Cells
Bone Marrow Transplantation
Cytotoxicity Tests, Immunologic
Female
Graft Rejection
Graft Survival
Immunization
Isoantibodies - biosynthesis
Kidney - immunology - physiology
Kidney Transplantation
Male
Rats
Rats, Inbred Lew
Skin Transplantation
Transplantation, Homologous
Abstract
Lewis rats that were given injections of 10(6) to 10(8) (Lewis X Brown Norway) F1 hybrid bone marrow cells produce predominantly, if not exclusively, 19S lymphocytotoxic antibodies. A number of Lewis rats that received transplants of perfused renal allografts from bone marrow donors at, or near, the peak of IgM response survival for well over 200 days with good renal function and no histological evidence of chronic rejection. All long-surviving rats had detectable lymphocytotoxic antibodies up to 120 days after allografting; late enhancing antibodies had the restricted specificity possibly identical or similar to anti-I region antisera. All rats bearing prolonged renal allografts were unable to accept donor-specific skin grafts or to respond with specific lymphocytotoxic antibodies following skin grafting. The possible involvement of non-complement-fixing 19S alloantibodies in active enhancement of rat renal allografts is discussed.
PubMed ID
324043 View in PubMed
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Alloantigen expression of a rat Moloney sarcoma.

https://arctichealth.org/en/permalink/ahliterature27934
Source
J Natl Cancer Inst. 1975 Oct;55(4):995-9
Publication Type
Article
Date
Oct-1975
Author
J M Jones
J D Feldman
Source
J Natl Cancer Inst. 1975 Oct;55(4):995-9
Date
Oct-1975
Language
English
Publication Type
Article
Keywords
Animals
Epitopes
Isoantigens - analysis
Moloney murine leukemia virus
Rats
Rats, Inbred BN
Rats, Inbred Lew
Rats, Inbred WF
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, U.S. Gov't, P.H.S.
Sarcoma, Experimental - immunology
Spleen - immunology
Abstract
Cells of a brown Norway (BN) rat Moloney sarcoma (MST) failed to express certain BN alloantigen specificities and bound only about 30-50% the amount of labeled alloantibody bound by normal BN spleen cells. MST cells lacked antigen specificities shared by BN and WF rats, but expressed some of the antigen shared by BN and AUG rats. Further loss of alloantigens that occurred with prolonged in vitro culture was associated with reduced virulence of MST cells for syngeneic hosts and with increased expression of tumor-associated antigens. The LEW rats, which are resistant to MST cells, might have rejected the tumor on the basis of factors other than Ag-B antigens.
PubMed ID
52723 View in PubMed
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alpha-Melanocyte-stimulating hormone protects the allograft in experimental heart transplantation.

https://arctichealth.org/en/permalink/ahliterature51606
Source
Transplantation. 2002 Dec 27;74(12):1678-84
Publication Type
Article
Date
Dec-27-2002
Author
Stefano Gatti
Gualtiero Colombo
Roberto Buffa
Flavia Turcatti
Letizia Garofalo
Nadia Carboni
Luca Ferla
Luigi R Fassati
James M Lipton
Anna Catania
Author Affiliation
Division of Liver Transplantation, Ospedale Maggiore di Milano IRCCS, Milano, Italy.
Source
Transplantation. 2002 Dec 27;74(12):1678-84
Date
Dec-27-2002
Language
English
Publication Type
Article
Keywords
Animals
Endothelin-1 - genetics
Gene Expression - drug effects
Graft Rejection - drug therapy - immunology - pathology
Graft Survival - drug effects - immunology
Heart Transplantation
Intercellular Adhesion Molecule-1 - genetics
Interferon Type II - genetics
Interleukin-1 - genetics
Male
Membrane Glycoproteins - genetics
Monocyte Chemoattractant Protein-1 - genetics
Nitrates - blood
Nitric Oxide - blood
Nitric Oxide Synthase - genetics
Nitric Oxide Synthase Type II
Nitrites - blood
Proto-Oncogene Proteins c-sis - genetics
RANTES - genetics
Rats
Rats, Inbred BN
Rats, Inbred Lew
Research Support, Non-U.S. Gov't
Transforming Growth Factor beta - genetics
Transplantation, Homologous
Tumor Necrosis Factor-alpha - genetics
Vascular Cell Adhesion Molecule-1 - genetics
alpha-MSH - pharmacology
Abstract
BACKGROUND: With the increasing need for organ transplantation and the use of "marginal" organs, novel approaches are sought to increase the efficiency and survival of transplanted tissue. We tested the idea that treatment with the anti-inflammatory peptide, alpha-melanocyte-stimulating hormone (alpha-MSH), an endogenous hormone that does not cause marked immunosuppression but does reduce reperfusion injury, may protect allografts and prolong their survival. METHODS: Donor cardiac grafts (Brown Norway) were transplanted heterotopically into the abdomen of recipient (Lewis) rats. Treatments consisted of intraperitoneal injections of Nle DPhe -alpha-MSH (NDP-alpha-MSH) or saline from the time of transplantation until sacrifice or spontaneous rejection. Allografts were removed on day 1, day 4, or at the time of rejection and examined for histopathology and expression of molecules prominent in reperfusion injury, transplant rejection, and apoptosis. RESULTS: NDP-alpha-MSH treatment caused a significant increase in allograft survival and a marked decrease in leukocyte infiltration. Expression of molecules such as endothelin 1, chemokines, and adhesion molecules, which are involved in allograft rejection, was significantly inhibited in NDP-alpha-MSH-treated rats. CONCLUSIONS: The results indicate that protection of the allograft from early injury with alpha-MSH can postpone rejection. Addition of this early protection with the peptide to usual treatment with immunosuppressive agents may, therefore, improve success of organ transplants.
PubMed ID
12499879 View in PubMed
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Antibody-induced restriction of viral gene expression in measles encephalitis in rats.

https://arctichealth.org/en/permalink/ahliterature57791
Source
J Virol. 1990 Feb;64(2):706-13
Publication Type
Article
Date
Feb-1990
Author
U G Liebert
S. Schneider-Schaulies
K. Baczko
V. ter Meulen
Author Affiliation
Institut für Virologie und Immunbiologie, Universität Würzburg, Federal Republic of Germany.
Source
J Virol. 1990 Feb;64(2):706-13
Date
Feb-1990
Language
English
Publication Type
Article
Keywords
Animals
Animals, Newborn
Antibodies, Monoclonal - immunology
Antibody formation
Blotting, Northern
Brain - microbiology
Encephalitis - immunology - microbiology
Female
Gene Expression Regulation, Viral
Genes, Viral
Measles - immunology
Measles virus - genetics - immunology - physiology
Nucleic Acid Hybridization
Pregnancy
RNA Probes
RNA, Messenger - analysis - genetics
RNA, Viral - isolation & purification
Rats
Rats, Inbred BN
Rats, Inbred Lew
Research Support, Non-U.S. Gov't
Spinal Cord - microbiology
Viral Structural Proteins - immunology
Virus Replication
Abstract
After infection with the neurotropic CAM/RBH measles virus (MV) strain, newborn Lewis rats succumb to an acute necrotizing encephalopathy. Passive transfer of neutralizing monoclonal antibodies directed against MV hemagglutinin prevented this disease process. Instead, either an antibody-induced acute or subacute measles encephalitis developed after a prolonged incubation period with a restricted expression of MV structural proteins. The molecular biological analysis of MV gene expression in brain tissue of rats treated with MV-neutralizing antibodies revealed a transcriptional restriction of viral mRNAs, particularly for the envelope proteins, leading to a steep expression gradient. Based on in situ hybridization, it was concluded that the efficiency of transcription of viral genes at the single-cell level is reduced compared with that of controls. Passive immunization with monoclonal antibodies directed against other MV structural proteins proved to be ineffective. Similar results were obtained in MV-infected weanling Brown Norway rats. These rats developed a clinically silent encephalitis in the presence of high titers of neutralizing antibodies. In such animals, a pronounced attenuation of the viral gene transcription was observed. These findings indicated that neutralizing antibodies directed against a restricted set of specific antigenic sites on the viral hemagglutinin protein expressed on cell membranes exert a modulating effect on the viral gene expression at the level of transcription. This phenomenon contributes to the switch from the acute cytopathic effect to a persistent infection in the central nervous system.
PubMed ID
2296081 View in PubMed
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Antigen-presenting cells in experimental autoimmune uveoretinitis.

https://arctichealth.org/en/permalink/ahliterature50954
Source
Exp Eye Res. 1998 Nov;67(5):539-48
Publication Type
Article
Date
Nov-1998
Author
S. Ishimoto
J. Zhang
V K Gullapalli
G. Pararajasegaram
N A Rao
Author Affiliation
Doheny Eye Institute and the Department of Ophthalmology, University of Southern California School of Medicine, California, 90033, USA.
Source
Exp Eye Res. 1998 Nov;67(5):539-48
Date
Nov-1998
Language
English
Publication Type
Article
Keywords
Adoptive Transfer
Animals
Antigen-Presenting Cells - immunology
Arrestin - immunology
Autoimmune Diseases - immunology - pathology
Bone Marrow Transplantation
Cell Line
Major Histocompatibility Complex
Pineal Gland - immunology
Rats
Rats, Inbred Lew
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Retinitis - immunology - pathology
T-Lymphocytes, Helper-Inducer - immunology
Transplantation Chimera
Uveitis - immunology - pathology
Abstract
The present study attempts to identify the antigen-presenting cells in the retina, utilizing bone marrow-transplanted chimeric rats. Two types of chimeras were used: one produced by transplanting bone marrow cells from F1 hybrids of Lewis and Brown Norway (BN) into sublethally irradiated Brown Norway rats (LBN/F1-->BN), followed by adoptive transfer of S-antigen-specific T cells obtained from Lewis rats; the second produced by transplanting bone marrow cells from BN rats into sublethally irradiated F1 hybrids (BN-->LBN/F1), followed by adoptive transfer of S-antigen-specific T cells obtained from F1 hybrids. As controls, Lewis, F1 hybrids and BN rats also received adoptive transfer of syngeneic uveitogenic T cell lines. All animals were killed on the seventh day after adoptive transfer and their eyes and pineal glands were analysed immunohistochemically, utilizing antibody directed against Lewis specific MHC class II molecules(OX-3). The analyses revealed the development of uveoretinitis and pinealitis in both types of chimeras and in the Lewis and F1 hybrid rats. BN rats did not develop uveoretinitis. OX-3-positive cells were found in the retina and the pineal glands of both types of chimeras, and in the Lewis and F1 hybrid rats but not in the BN rats. These cells in the retina expressed dendritic morphology and perivascular distribution. Retinal pigment epithelia, Müller cells and the vascular endothelia of both chimeras, the two strains, and the F1 hybrid rats did not demonstrate OX-3-positive staining. These results suggest that the bone marrow-derived cells in the retina and pineal gland may present S-antigen to T cells, initiating the cascade of uveoretinitis and pinealitis.
PubMed ID
9878216 View in PubMed
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Anti-inflammatory effects of a cyclosporine receptor-binding compound, D-43787.

https://arctichealth.org/en/permalink/ahliterature13971
Source
J Pharmacol Exp Ther. 2002 May;301(2):738-46
Publication Type
Article
Date
May-2002
Author
Andreas Pahl
Meixia Zhang
Katalin Török
Hildegard Kuss
Ute Friedrich
Zoltan Magyar
Jozsef Szekely
Katalin Horvath
Kay Brune
Istvan Szelenyi
Author Affiliation
Department of Experimental and Clinical Pharmacology and Toxicology, University of Erlangen-Nürnberg, Erlangen, Germany.
Source
J Pharmacol Exp Ther. 2002 May;301(2):738-46
Date
May-2002
Language
English
Publication Type
Article
Keywords
Animals
Anti-Inflammatory Agents - pharmacology - therapeutic use
Arthritis, Experimental - drug therapy
Asthma - prevention & control
Cell Division - drug effects
Cyclophilin A - drug effects - metabolism
Cyclosporine - pharmacology
Cytokines - metabolism
Disease Models, Animal
Dose-Response Relationship, Drug
Guinea Pigs
Humans
Immunosuppressive Agents - pharmacology - therapeutic use
Indoles - chemistry - pharmacology - therapeutic use
Injections, Intraperitoneal
Injections, Subcutaneous
Leukocytes, Mononuclear - cytology - drug effects
Lysine - analogs & derivatives - chemistry - pharmacology - therapeutic use
Male
Peptidylprolyl Isomerase - metabolism
Rats
Rats, Inbred BN
Rats, Inbred Lew
Research Support, Non-U.S. Gov't
Th1 Cells - drug effects - metabolism
Th2 Cells - drug effects - metabolism
Abstract
By virtue of its binding to cyclophilin, the cellular receptor for cyclosporine (CsA), we could identify a new compound D-43787 [N-[(1-tert-butyloxycarbonyl)-indolin-2-(S)-carbonyl]-indolin-2-(S)-carbonacid-[N-epsilon-benzyloxycarbonyl)-2-(S)-lysin methylester]-amide] exhibiting immunomodulating properties. It inhibited cell proliferation induced by 12-O-tetradecanoylphorbol-13-acetate (TPA)/ionomycin and anti-CD3/CD28 with an IC(50) of 0.3 microM. The protein phosphatase calcineurin, which is the target of the CsA-cyclophilin complex, is not inhibited by D-43787. It inhibited T helper cell (Th) 2 cytokines interleukin (IL)-4, -5, and -13 more effectively than the Th1 cytokine interferon (IFN)-gamma in human primary T cells. The IC(50) for IL-5 and IL-13 in TPA/ionomycin-stimulated peripheral blood mononuclear cells (PBMC) is 0.7 +/- 0.1 and 0.5 +/- 0.1 microM, respectively, whereas the IC(50) for IFN-gamma is 2.0 +/- 0.4 microM. When PBMC were stimulated with anti-CD3/CD28, the IC(50) for IL-4, -5, and -13 were 1.5 +/- 0.2, 1.8 +/- 0.2, and 1.9 +/- 0.4 microM, respectively. IFN-gamma was only partially inhibited under these conditions. This effect was even more pronounced in pure CD4(+) T cells. Pretreatment of human monocytes with D-43787 inhibited lipopolysaccharide-induced proinflammatory cytokines IL-6 and TNFalpha with an IC(50) of 1.2 +/- 0.1 and 4.7 +/- 0.9 microM, respectively. In vivo, D-43787 potently inhibited late-phase eosinophilia in actively sensitized and challenged guinea pigs (10 mg/kg, i.p.: 51%) and Brown-Norway rats (1 mg/kg, intrapulmonary: 66% 30 mg/kg, i.p.: 50%). In adjuvant-induced arthritis, D-43787 (10-40 mg/kg, b.i.d., i.p.) dose dependently reduced edema development on both hind paws. The potency of D-43787 was comparable with that of indomethacin and dexamethasone. In conclusion, we characterized a novel Th2 selective immunosuppressive drug with possible anti-asthmatic/anti-inflammatory effects. Its mode of action is distinct from that of CsA.
PubMed ID
11961080 View in PubMed
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189 records – page 1 of 19.