DOCSLIB.ORG

Hematopoietic Stem-Cell Defects Underlying Abnormal Macrophage Development and Maturation in NOD/Lt Mice

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Hematopoietic Stem-Cell Defects Underlying Abnormal Macrophage Development and Maturation in NOD/Lt Mice Proc. Natl. Acad. Sci. USA Vol. 90, pp. 9625-9629, October 1993 Immunology Hematopoietic stem-cell defects underlying abnormal macrophage development and maturation in NOD/Lt mice: Defective regulation of cytokine receptors and protein kinase C DAVID V. SERREZE, JENS W. GAEDEKE, AND EDWARD H. LEITER* The Jackson Laboratory, 600 Main Street, Bar Harbor, ME 04609 Communicated by Elizabeth S. Russell, July 19, 1993 ABSTRACT The immunopathogenesis of autoimmune in- I-Ek, Db) of NON blocked the development of diabetogenic sulin-dependent diabetes in NOD mice entails defects in the T cells from NOD bone marrow (4). In addition, the inability development of macrophages (M$s) from hematopoietic pre- of NOD APCs to activate immunoregulatory T cells in a cursors. The present study analyzes the cellular and molecular syngeneic mixed-lymphocyte reaction was also found to be basis underlying our previous finding that the MO growth associated with homozygous expression of H-2g7 (5). factor colony-stimulating factor 1 (CSF-1) promotes a reduced Interactions between the H-2g7 haplotype and non-MHC- level of promonocyte proliferation and MO development from linked background genes also underlie the MO developmental NOD bone marrow. CSF-1 stimulation of NOD marrow in- anomalies characteristic of NOD mice. NOD bone marrow duced Mos to differentiate to the point that they secreted levels cells proliferate poorly in response to several myeloid growth of tumor necrosis factor a equivalent to that of controls. factors (6, 7). The myeloid growth factor, colony-stimulating However, CSF-1 failed to prime NOD M$s to completely factor 1 (CSF-1) generates fewer phenotypically mature differentiate in response to y-interferon, as shown by their (Mac-3+) M6s from NOD marrow than from diabetes- decreased lipopolysaccharide-stimulated interleukin 1 secre- resistant strains (6). This is consistent with the finding that tion. These defects, in turn, were associated with an inability peritoneal Mos from NOD mice are poor interleukin 1 (IL-1) of CSF-1 to up-regulate c-fms (CSF-1 receptor) and Ifgr secretors (5, 8), since M0s reportedly do not acquire the (y-interferon receptor) expression. Even though the combina- ability to secrete IL-1,8 until the later stages ofdifferentiation tion of CSF-1 and y-interferon up-regulated c-fins and Ifgr (9). Further evidence for dysregulated monocyte function in transcript levels in NOD M#s to levels induced in control M$s NOD mice is reflected by the aberrant responses of cells in by CSF-1 alone, the protein kinase C activities coupled to these this lineage to y-interferon (IFN-y) stimulation. As expected, receptors remained 4-fold lower in NOD M#s than in Mos IFN-y, which induces MO differentiation and activation, derived from the marrow of diabetes-resistant NON and SWR inhibited CSF-1-stimulated proliferation of bone marrow control mice. Despite expressing the diabetogenic H-2g7 hap- cells from diabetes-resistant strains (6). In contrast, IFN-y lotype, Mos derived from cytokine-stimulated marrow of the aberrantly increased CSF-1-stimulated proliferation of NOD NON.H-2g7 congenic stock were functionally more mature than bone marrow cells and increased the number of Mac-3+ similarly derived Ms%s from NOD mice. Whereas diabetes progeny generated to levels equivalent to that produced from resistance was abrogated in 67% of irradiated (NOD x the marrow of control strains stimulated with CSF-1 alone NON)F1 females reconstituted with NOD marrow, no recipi- (6). In addition, as a result of defects in background-specific ents became diabetic after reconstitution with a 1:1 mixture of trans-regulatory factors, IFN- y also aberrantly down- marrow from NOD and the congenic stock. Thus, failure to regulated H-2g7 MHC class I expression in NOD peritoneal develop functionally mature monocytes may be of pathogenic Mos (6). Collectively, these results indicate that non-MHC- significance in NOD mice. linked genes either independently or through interaction with the diabetogenic H-2g7 haplotype contribute to impairments NOD is an inbred mouse strain characterized by a high in monocyte differentiation and function in NOD mice. incidence of T-cell-mediated autoimmune insulin-dependent Antigens that are processed and presented in an ineffi'cient diabetes (1). Genetic outcross of NOD with the closely fashion can continue to stimulate T-cell proliferative re- related but diabetes-resistant NON inbred strain has shown sponses in the periphery but are unable to induce tolerance that diabetogenesis results from complex polygenic interac- (10, 11). Similarly, activation-driven T-cell death requires tions between the rare H-2g7 major histocompatibility com- quantitatively more antigenic stimulation than is required to plex (MHC) haplotype (Kd, I-AM7, I-Enuil, Db) of NOD and trigger T-cell proliferation (12). In addition, the stimulation of non-MHC-linked susceptibility modifiers (2). These diabeto- immunoregulatory T cells requires a more highly activated genic interactions are initiated at the hematopoietic stem-cell APC than is required to trigger effector T cells (13). Thus, in level since diabetes resistance in (NOD x NON)F1 hybrids synergy with the diabetogenic H-2 7 haplotype, the non- is abrogated by lethal irradiation and reconstitution with defects in NOD bone marrow but not NON/Lt or F1 bone marrow (3, MHC-linked background genes contributing to MO 4). Several lines of evidence indicate that H-297-expressing development may contribute to diabetogenesis in NOD mice antigen-presenting cells (APCs), such as macrophages (M0s) by decreasing the ability of APCs to process and/or present derived from NOD stem cells, fail to mediate the clonal (-cell autoantigens in a manner quantitatively sufficient to deletion of f-cell autoreactive T cells and/or to activate induce tolerance. Therefore, the present study was con- immunoregulatory T cells. These include the finding that ducted to assess the functional consequences ofimpaired MO marrow-derived APCs, but not thymic epithelial cells, ex- pressing the diabetes-resistant H-2nbl haplotype (Kb, I-Anbl, Abbreviations: APC, antigen-presenting cell; CSF-1, colony- stimulating factor 1; IFN-y, y-interferon; IL-1, interleukin 1; LPS, lipopolysaccharide; MO, macrophage; MHC, major histocompatibil- The publication costs ofthis article were defrayed in part by page charge ity complex; PKC, protein kinase C; TNF-a, tumor necrosis factor payment. This article must therefore be hereby marked "advertisement" a. in accordance with 18 U.S.C. §1734 solely to indicate this fact. *To whom reprint requests should be addressed. 9625 Downloaded by guest on September 27, 2021 9626 Immunology: Serreze et al. Proc. Natl. Acad. Sci. USA 90 (1993) development in NOD mice and to analyze the mechanisms washed with 75 mM phosphoric acid and 75 mM sodium underlying these maturational defects. phosphate (pH 7.5), and then radioactivity was measured in a 8 scintillation counter (LKB) to assess PKC-driven phos- MATERIALS AND METHODS phorylation of the synthetic substrate. Data are presented as cpm (mean ± SEM) corrected for nonspecific 32p incorpo- Mice. NOD/Lt and NON/Lt mice have been maintained in ration obtained in the absence of substrate and for the protein our research colony by brother-sister mating since being concentration of the reaction supernatant. obtained from George Eisenbarth (Joslin Diabetes Center, Competitive Bone Marrow Reconstitution Studies. Diabe- Boston) at the 32nd and 35th generation of inbreeding, tes-resistant (NOD x NON)F1 female mice were lethally respectively. The previously described (2, 14) diabetes- irradiated (1000R; 1R = 0.258 mC/kg) at 4 weeks of age and resistant NOD.NON-H-2nbl (designated NOD.H-2nbl) and reconstituted as described (4) with a 1:1 mixture of T-cell- NON.NOD-H-2g7 congenic strains (designated NON.H-2g7) depleted NOD and NON.H-2g7 bone marrow cells (2.5 x 106 were utilized at the 21st and 13th backcross generations, marrow cells from each strain). Controls consisted of F1 respectively. SWR/Bm (H-2q) mice were kindly supplied by hybrids reconstituted with NOD bone marrow alone. Chi- Wesley Beamer (The Jackson Laboratory). Nondiabetic fe- meras were monitored through 40 weeks of age for the male mice between 8 and 12 weeks of age were used for all development ofglycosuria with Tes-Tape (kindly supplied by experiments and were maintained under specific pathogen- Eli Lilly). Upon diabetes onset or reaching 40 weeks of age, free conditions and allowed free access to food (diet 96W, splenocytes from the chimeras were typed as described (4, Emory Morse, Guilford, CT) and acidified drinking water. 22) by two-color flow cytometric analysis with the Thy-1.2 IL-1 and Tumor Necrosis Factor a (TNF-ea) Production by (NOD type)-specific monoclonal antibody HO13-4.9 and the Bone Marrow-Derived Mos. Bone marrow cells were sus- Thy-1.1 (NON.H-2g7 type)-specific monoclonal antibody pended at 2.0 x 106 cells per ml in culture medium (5) HO22-1 to estimate the percentage of leukocytes derived containing recombinant human CSF-1 (Cetus) at 500 units/ml from each marrow population. with and without recombinant rat IFN-y at 10 units/ml (kindly supplied by P. van de Meide, Rijswijk, The Nether- lands) and cultured for 4 days at 37°C in a humidified 5% RESULTS C02/95% air atmosphere. The proliferative responses and Comparison ofIL-1 and TNF-a Secretion by Bone Marrow- level ofMac-3 expression ofthe cells emanating from marrow Derived M#s from NOD Mice and Diabetes-Resistant Strains. cultured with this source and concentration of CSF-1 were Fig. 1 compares LPS-stimulated IL-1 secretion of Mis de- found to be equivalent to that induced by CSF-1 at 25 rived from NOD marrow cultured in CSF-1 with and without units/ml [obtained from Genzyme-the CSF-1 used in our IFN-y to that of similarly derived Mis from diabetes- previous study (6)].
Load more

Recommended publications
  • Chapter 18 *Lecture Powerpoint the Circulatory System: Blood
    Chapter 18 *Lecture PowerPoint The Circulatory System: Blood *See separate FlexArt PowerPoint slides for all figures and tables preinserted into PowerPoint without notes. Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Introduction • Many myths about blood – Mysterious ―vital force‖ – Drained ―bad-blood‖ for medical reasons – Hereditary traits were once thought to be transmitted through blood • Blood cells were seen with the first microscopes • Hematology—the study of blood • Recent developments in this field help save lives 18-2 Introduction • Expected Learning Outcomes – Describe the functions and major components of the circulatory system. – Describe the components and physical properties of blood. – Describe the composition of blood plasma. – Explain the significance of blood viscosity and osmolarity. – Describe in general terms how blood is produced. 18-3 Functions of the Circulatory System • Circulatory system consists of the heart, blood vessels, and blood • Cardiovascular system refers only to the heart and blood vessels • Hematology—the study of blood • Functions of circulatory system – Transport • O2, CO2, nutrients, wastes, hormones, and stem cells – Protection • Inflammation, limit spread of infection, destroy microorganisms and cancer cells, neutralize toxins, and initiate clotting – Regulation • Fluid balance, stabilizes pH of ECF, and temperature control 18-4 Components and General Properties of Blood • Adults have 4 to 6 L of blood • A liquid connective tissue consisting of
    [Show full text]
  • Of THP-1 Acute Monocytic Leukemia Cells Halt Proliferation and Induce
    Human Plasma Membrane-Derived Vesicles Halt Proliferation and Induce Differentiation of THP-1 Acute Monocytic Leukemia Cells This information is current as Ephraim A. Ansa-Addo, Sigrun Lange, Dan Stratton, of September 28, 2021. Samuel Antwi-Baffour, Igor Cestari, Marcel I. Ramirez, Maria V. McCrossan and Jameel M. Inal J Immunol 2010; 185:5236-5246; Prepublished online 4 October 2010; doi: 10.4049/jimmunol.1001656 Downloaded from http://www.jimmunol.org/content/185/9/5236 References This article cites 43 articles, 12 of which you can access for free at: http://www.jimmunol.org/content/185/9/5236.full#ref-list-1 http://www.jimmunol.org/ Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists by guest on September 28, 2021 • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2010 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Human Plasma Membrane-Derived Vesicles Halt Proliferation and Induce Differentiation of THP-1 Acute Monocytic Leukemia Cells Ephraim A.
    [Show full text]
  • White Blood Cells)
    Lec.4 Medical Physiology – Blood Physiology Z.H.Kamil Leukocytes (White Blood Cells) Leukocytes are the only formed elements that are complete cells, with nuclei and the usual organelles. Accounting for less than 1% of total blood volume, leukocytes are far less numerous than red blood cells. On average, there are 4800–10,800 WBCs/μl of blood. Leukocytes are crucial to our defense against disease. They form a mobile army that helps protect the body from damage by bacteria, viruses, parasites, toxins, and tumor cells. As such, they have special functional characteristics. Red blood cells are kept into the bloodstream, and they carry out their functions in the blood. But white blood cells are able to slip out of the capillary blood vessels in a process called diapedesis and the circulatory system is simply their means of transport to areas of the body (mostly loose connective tissues or lymphoid tissues) where they mount inflammatory or immune responses. The signals that prompt WBCs to leave the bloodstream at specific locations are cell adhesion molecules displayed by endothelial cells forming the capillary walls at sites of inflammation. Once out of the bloodstream, leukocytes move through the tissue spaces by amoeboid motion (they form flowing cytoplasmic extensions that move them along). By following the chemical trail of molecules released by damaged cells or other leukocytes, a phenomenon called positive chemotaxis, they pinpoint areas of tissue damage and infection and gather there in large numbers to destroy foreign substances and dead cells. Whenever white blood cells are mobilized for action, the body speeds up their production and their numbers may double within a few hours.
    [Show full text]
  • Download As A
    QUANTITATIVE STUDY ON THE PRODUCTION AND KINETICS OF MONONUCLEAR PHAGOCYTES DURING AN ACUTE INFLAMMATORY REACTION BY RALPH VAN FURTH, MARTINA M. C. DIESSELHOFF-DEN DULK, AND HERMAN MATTIE* (From the Department of Microbial Diseases, University Hospital, Leiden, The Netherlands) (Received for publication 10 July 1973) During an acute inflammatory response in the peritoneal cavity both the peritoneal macrophages and the monocytes in the peripheral blood increase in number (1, 2). Labeling studies with [3H]thyrnidine have demonstrated that during an acute inflam- mation, just as during the normal steady state, the peritoneal macrophages derive from peripheral blood monocytes (1), which originate in the bone marrow from divid- ing promonocytes (3, 4). Although the mitotic activity of the promonocytes (DNA-synthesis time and cell cycle time) and the kinetic characteristics of these cells have been studied quantita- tively under steady-state conditions (4) and during treatment with glucocortico- steroids (5), similar data are not available for the acute inflammatory response. The present quantitative study, performed during an acute inflammation, provided data on the production of monocytes in the bone marrow, the influx and efflux of these cells into and from the peripheral blood, and the migration of monocytes into inflammatory lesion of the peritoneal cavity. These results were compared with the findings during the normal steady state. Materials and Methods Animals.--Specific pathogen-free male Swiss mice weighing 25-30 g (Central Institute for the Breeding of Laboratory Animals, TNO, Bilthoven, The Netherlands) were used. Cell Cultures.--The techniques for harvesting and culturing mouse bone marrow cells and peritoneal macrophages have been described in detail elsewhere (1, 3).
    [Show full text]
  • Platelet-Rich Plasma Regenerative Medicine: Sports Medicine, Orthopedic, and Recovery of Musculoskeletal Injuries Lecture Notes in Bioengineering
    Lecture Notes in Bioengineering José Fábio Santos Duarte Lana Maria Helena Andrade Santana William Dias Belangero Angela Cristina Malheiros Luzo Editors Platelet-Rich Plasma Regenerative Medicine: Sports Medicine, Orthopedic, and Recovery of Musculoskeletal Injuries Lecture Notes in Bioengineering For further volumes: http://www.springer.com/series/11564 José Fábio Santos Duarte Lana Maria Helena Andrade Santana William Dias Belangero • Angela Cristina Malheiros Luzo Editors Platelet-Rich Plasma Regenerative Medicine: Sports Medicine, Orthopedic, and Recovery of Musculoskeletal Injuries 123 Editors José Fábio Santos Duarte Lana William Dias Belangero Research Institute of Sports Medicine Department of Orthopaedic and Orthopedics and Regeneration—iMOR Traumatology, Faculty of Medical Uberaba, MG Sciences Brazil University of Campinas Campinas, SP and Brazil Member of the Regenerative Angela Cristina Malheiros Luzo and Cell Therapy Group, Hemocentro Haematology and Hemotherapy Center University of Campinas, Unicamp Umbilical Cord Blood Bank Campinas, SP University of Campinas Brazil Campinas, SP Brazil Maria Helena Andrade Santana Department of Materials and Bioprocesses Engineering, School of Chemical Engineering University of Campinas Campinas, SP Brazil ISSN 2195-271X ISSN 2195-2728 (electronic) ISBN 978-3-642-40116-9 ISBN 978-3-642-40117-6 (eBook) DOI 10.1007/978-3-642-40117-6 Springer Heidelberg New York Dordrecht London Library of Congress Control Number: 2013950744 Ó Springer-Verlag Berlin Heidelberg 2014 This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed.
    [Show full text]
  • 10 11 Cyto Slides 81-85
    NEW YORK STATE CYTOHEMATOLOGY PROFICIENCY TESTING PROGRAM Glass Slide Critique ~ November 2010 Slide 081 Diagnosis: MDS to AML 9 WBC 51.0 x 10 /L 12 Available data: RBC 3.39 x 10 /L 72 year-old female Hemoglobin 9.6 g/dL Hematocrit 29.1 % MCV 86.0 fL Platelet count 16 x 109 /L The significant finding in this case of Acute Myelogenous Leukemia (AML) was the presence of many blast forms. The participant median for blasts, all types was 88. The blast cells in this case (Image 081) are large, irregular in shape and contain large prominent nucleoli. It is difficult to identify a blast cell as a myeloblast without the presence of an Auer rod in the cytoplasm. Auer rods were reported by three participants. Two systems are used to classify AML into subtypes, the French- American-British (FAB) and the World Health Organization (WHO). Most are familiar with the FAB classification. The WHO classification system takes into consideration prognostic factors in classifying AML. These factors include cytogenetic test results, patient’s age, white blood cell count, pre-existing blood disorders and a history of treatment with chemotherapy and/or radiation therapy for a prior cancer. The platelet count in this case was 16,000. Reduced number of platelets was correctly reported by 346 (94%) of participants. Approximately eight percent of participants commented that the red blood cells in this case were difficult to evaluate due to the presence of a bluish hue around the red blood cells. Comments received included, “On slide 081 the morphology was difficult to evaluate since there was a large amount of protein surrounding RBC’s”, “Slide 081 unable to distinguish red cell morphology due to protein” and “Unable to adequately assess morphology on slide 081 due to poor stain”.
    [Show full text]
  • 10 Maturation and Development of Leucocytes
    MODULE Maturation and Development of Leucocytes Hematology and Blood Bank Technique 10 Notes MATURATION AND DEVELOPMENT OF LEUCOCYTES 10.1 INTRODUCTION The leucocytes develop from the multipotent hematopoietic stem cell which then gives rise to a stem cell committed to formation of leucocytes. Both these cells cannot be identified morphologically by routine methods. The various types of leucocytes are granulocytes (neutrophils, eosinophils and basophils), monocytes and lymphocytes. The three cell types develop separately and accordingly these processes will be discussed separately. OBJECTIVES After reading this lesson, you will be able to: z explain the various stages in the development of leucocytes. z describe the different types of leucocytes seen normally in PBF. 10.2 MYELOPOIESIS This is the process of formation of myeloid cells. It is restricted to the bone marrow after birth. The committed progenitor cell for granulocytes and monocytes is the GM-CFU which proliferates and differentiates to form myeloblast and monoblast. The myeloblast is the earliest morphologically identifiable cell. It is 10-18µm in size. The cytoplasm is scant and basophilic, usually agranular and may contain a few azurophilic cytoplasmic granules in the blast transiting to the next stage 80 HEMATOLOGY AND BLOOD BANK TECHNIQUE Maturation and Development of Leucocytes MODULE of promyelocyte. It has a large round to oval nucleus with a smooth nuclear Hematology and Blood membrane. The chromatin is fine, lacy and is evenly distributed throughout the Bank Technique nucleus. Two-five nucleoli can be identified in the nucleus. The next stage of maturation is the Promyelocyte. It is larger than a myeloblast, 12-20 µm with more abundant cytoplasm which has abundant primary azurophilic granules .
    [Show full text]
  • Clotting Factors Secreted by Monocytes and Macrophages
    Clotting factors secreted by monocytes and macrophages Citation for published version (APA): van Dam-Mieras, M. C. E., Muller, A. D., van Deijk, W. D., & Hemker, H. C. (1985). Clotting factors secreted by monocytes and macrophages: Analytical considrations. Thrombosis Research, 37(1), 9-19. https://doi.org/10.1016/0049-3848(85)90028-3 Document status and date: Published: 01/01/1985 DOI: 10.1016/0049-3848(85)90028-3 Document Version: Publisher's PDF, also known as Version of record Please check the document version of this publication: • A submitted manuscript is the version of the article upon submission and before peer-review. There can be important differences between the submitted version and the official published version of record. People interested in the research are advised to contact the author for the final version of the publication, or visit the DOI to the publisher's website. • The final author version and the galley proof are versions of the publication after peer review. • The final published version features the final layout of the paper including the volume, issue and page numbers. Link to publication General rights Copyright and moral rights for the publications made accessible in the public portal are retained by the authors and/or other copyright owners and it is a condition of accessing publications that users recognise and abide by the legal requirements associated with these rights. • Users may download and print one copy of any publication from the public portal for the purpose of private study or research. • You may not further distribute the material or use it for any profit-making activity or commercial gain • You may freely distribute the URL identifying the publication in the public portal.
    [Show full text]
  • By P-Selectin Glycoprotein Ligand 1 Through a Juxtacrine Mechanism
    Follicular Dendritic Cells Activate HIV-1 Replication in Monocytes/Macrophages through a Juxtacrine Mechanism Mediated by P-Selectin Glycoprotein Ligand 1 This information is current as of September 24, 2021. Kenji Ohba, Akihide Ryo, Md. Zahidunnabi Dewan, Mayuko Nishi, Toshio Naito, Xiaohua Qi, Yoshio Inagaki, Yoji Nagashima, Yuetsu Tanaka, Takashi Okamoto, Kazuo Terashima and Naoki Yamamoto J Immunol 2009; 183:524-532; ; Downloaded from doi: 10.4049/jimmunol.0900371 http://www.jimmunol.org/content/183/1/524 http://www.jimmunol.org/ Supplementary http://www.jimmunol.org/content/suppl/2009/06/18/183.1.524.DC1 Material References This article cites 54 articles, 17 of which you can access for free at: http://www.jimmunol.org/content/183/1/524.full#ref-list-1 Why The JI? Submit online. by guest on September 24, 2021 • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2009 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Follicular Dendritic Cells Activate HIV-1 Replication in Monocytes/Macrophages through a Juxtacrine Mechanism Mediated by P-Selectin Glycoprotein Ligand 11 Kenji Ohba,*† Akihide Ryo,2* Md.
    [Show full text]
  • PHYSIOLOGY I 2018-2019 Hematology
    PHYSIOLOGY I 2018-2019 Prof.Dr.Çiğdem ALTINSAAT Hematology Blood as a system Function of Blood-Blood is a type of liquid connective tissue and is specialized fluid of connective tissue. Contains cells suspended in a fluid matrix The major function of blood is transport. Subfunctions Respiration :-if oxygen and carbon dioxide are transported Trophic : -when the nutrient materials are delivered to the tissues Excretive : -when the metabolites are delivered from tissues to excretory organs Regulative : if the hormones and BAS are transported Homeostatic :maintenance of water content and acid-basebalance Protective : immunity and non-specific resistance; blood coagulation Maintenance of body temperature :-as a result of a redistribution of blood volume between skin and the internal organs at high and low temperature of external environment. Blood (peripheral circulating) Organs for haemopoiesis destruction of blood Regulatory apparatus (nervous and humoral) The total blood volume makes up about 6-8 percent (1/13) of the body’s weight in human, 1/15 in horse, 1/12 in cow, 1/13 in dog and sheep, 1/22 in pig, 1/20 in cat, rabbit and guinea pig. Accordingly, a 70-kilogram person will have 5 to 6 litres of blood. Circulating blood volume will be lesser than total blood volume, because some amount of blood will be deposited in organs like liver. General Characteristics of Blood 38°C (100.4°F) is normal temperature High viscosity Slightly alkaline pH (7.35–7.45) Blood composition Blood consists of liquid plasma (volume-55-60%) formed elements (cells) (volume-40-45%) Formed elements include 1.
    [Show full text]
  • Monocytes, Macrophages, and Their Diseases in Man
    oo22-202X/ 78/ 7101-0056$02.oo/ 0 THE Jo fiNA L O F INVESTIGATIVE DERMATOLOGY, 71:56-58,1978 Vol. 71, NO.1 Copyright © 1978 by The Williams & Wilkins Co. Printed in U.S.A. I Monocytes, Macrophages, and Their Diseases in Man MARTiN J. CLINE, M.D. Division of Hematology-Oncology, Department of Medicine, University of California School of Medicine, Los Angeles, California, U.S.A. Mononuclear phagocytes are a widely distributed sys­ pool in a ratio of 1:3, (iii) monocytes leave the blood exponen­ tem of cells involved in host defense functions, immu­ tially with a half life of 8.4 hr, (iv), the half life may be prolonged nologic reactions, disposal of unwanted organic and in­ in patients with monocytosis and shortened in patients with \ organic materials, and synthesis of biologically active acute infection or splenomegaly, and (v) the normal monocyte compounds such as complement components and pros­ turnover rate averages 7 X lOG cells pel' hour pel' kilogram of taglandins. The system includes early precursor cells in body weight. the bone marrow, blood monocytes, alveolar and peri­ Available data suggest that there is no significant reentry of toneal macrophages, sinusoidal lining cells in the spleen, monocytes into the bloodstream once they have left the circu­ and Kupffer cells in the liver. We have recently come to lation. They enter the tissues and mature to macrophages. The understand the biology of these interesting cells and the major source of mononuclear phagocytes accumulating at in­ diseases they produce. flammatory foci is the monocyte precursors of the bone marrow [6].
    [Show full text]
  • 1. Red Blood Cells (Rbcs) Or Erythrocytes
    An Introduction to Blood and the Cardiovascular System • The Cardiovascular System consists of: • A pump (the heart) • A conducting system (blood vessels) • A fluid medium (blood) • Is specialized fluid of connective tissue • Contains cells suspended in a fluid matrix © 2012 Pearson Education, Inc. An Introduction to Blood and the Cardiovascular System • Blood • Transports materials to and from cells • Oxygen and carbon dioxide • Nutrients • Hormones • Immune system components • Waste products © 2012 Pearson Education, Inc. 19-1 Physical Characteristics of Blood • Important Functions of Blood • Transportation of dissolved substances • Regulation of pH and ions • Restriction of fluid losses at injury sites • Defense against toxins and pathogens • Stabilization of body temperature © 2012 Pearson Education, Inc. 19-1 Physical Characteristics of Blood • Whole Blood • Plasma • Fluid consisting of: • Water • Dissolved plasma proteins • Other solutes • Formed elements • All cells and solids © 2012 Pearson Education, Inc. Figure 19-1 The Composition of Whole Blood 7% Plasma Plasma Proteins 1% Other Solutes 46–63% Water 92% Formed Elements Platelets < .1% White Blood Cells 37–54% Red Blood Cells < .1% 99.9% © 2012 Pearson Education, Inc. 19-1 Physical Characteristics of Blood • Three Types of Formed Elements 1. Red blood cells (RBCs) or erythrocytes • Transport oxygen 2. White blood cells (WBCs) or leukocytes • Part of the immune system 3. Platelets • Cell fragments involved in clotting © 2012 Pearson Education, Inc. 19-1 Physical Characteristics of Blood • Hemopoiesis • Process of producing formed elements • By myeloid and lymphoid stem cells • Fractionation • Process of separating whole blood for clinical analysis • Into plasma and formed elements © 2012 Pearson Education, Inc. 19-1 Physical Characteristics of Blood • Three General Characteristics of Blood 1.
    [Show full text]