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Journal articles on the topic 'Polyclonale'

Author: Grafiati

Published: 7 December 2024

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1

Larbouret, Christel, Marie-Alix Poul, and Thierry Chardès. "Imiter la réponse immunitaire humorale polyclonale." médecine/sciences 35, no. 12 (December 2019): 1083–91. http://dx.doi.org/10.1051/medsci/2019216.

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Les anticorps monoclonaux ont révolutionné le traitement de nombreuses maladies mais leur efficacité clinique reste limitée dans certains cas. Des associations d’anticorps se liant à une même cible (homo-combinaisons) ou à plusieurs cibles différentes (hétéro-combinaisons), mimant ainsi une réponse immunitaire humorale polyclonale, ont conduit à une amélioration thérapeutique dans des essais précliniques et cliniques, essentiellement en cancérologie et en infectiologie. Ces combinaisons augmentent l’efficacité des réponses biologiques et court-circuitent les mécanismes de résistances observés lors d’une monothérapie par anticorps. Le procédé de formulation et d’administration des combinaisons d’anticorps le plus fréquent est une formulation séparée, avec injection séquentielle de chaque anticorps « principe actif ». Alternativement, se développent des formulations combinées, où les anticorps produits séparément sont mélangés avant administration, ou produits simultanément par une lignée cellulaire unique ou un mélange de lignées cellulaires correspondant à une master-bank cellulaire polyclonale. La réglementation, la toxicité et la séquence d’injection des mélanges oligoclonaux restent des points à éclaircir et à optimiser pour un meilleur effet thérapeutique.

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2

Le Lostec, Z., P. Mornet, H. Mossafa, F. Drupt, V. Asnafi, E. de Raucourts, and J. Y. Peltier. "Lymphocytose polyclonale persistante chez une femme tabagique." La Revue de Médecine Interne 23 (May 2002): 127s—128s. http://dx.doi.org/10.1016/s0248-8663(02)80260-0.

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3

Belmecheri, F., A. Benyamine, A. Murati, J. M. Schiano De Colella, D. Olive, R. Bouabdallah, and P. J. Weiller. "La lymphocytose T polyclonale, un syndrome parathymique très rare." La Revue de Médecine Interne 38 (June 2017): A213—A214. http://dx.doi.org/10.1016/j.revmed.2017.03.316.

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4

de Jaureguiberry, J. P., D. Pignon, M. Galzin, P. Carli, D. Jaubert, and A. Chagnon. "Lymphocytose B polyclonale persistante à lymphocytes binucléés chez un homme." La Revue de Médecine Interne 18, no. 3 (March 1997): 258. http://dx.doi.org/10.1016/s0248-8663(97)89307-1.

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5

Théodose, Raphaëlle, Georges Jung, Anne Debecker, Valérie Gauduchon, and Philippe Hénon. "Cas clinique au laboratoire hyperlymphocytose chronique polyclonale à noyaux binucléés." Revue Française des Laboratoires 1998, no. 307 (November 1998): 75–77. http://dx.doi.org/10.1016/s0338-9898(98)80223-0.

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6

Garrigues, P., M. H. Tugler, C. Jockey, and D. Champetier de Ribes. "Anémie hémolytique auto-immune révélant une lymphocytose polyclonale à lymphocytes binucléés." La Revue de Médecine Interne 34 (December 2013): A121—A122. http://dx.doi.org/10.1016/j.revmed.2013.10.210.

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7

Guignant, C., A. Mambie, M. Diouf, C. Roumier, C. Roche-Lestienne, B. Gruson, B. Gubler, et al. "Lymphocytose polyclonale à lymphocytes binucléés : une cause de déficit immunitaire humoral ?" La Revue de Médecine Interne 37 (June 2016): A49—A50. http://dx.doi.org/10.1016/j.revmed.2016.04.256.

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8

Soetart, Nicolas, and Laetitia Jaillardon. "Caractériser une gammapathie : intérêts de l’immunoélectrophorèse." Le Nouveau Praticien Vétérinaire canine & féline 16, no. 72 (2019): 65–67. http://dx.doi.org/10.1051/npvcafe/72065.

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De nombreuses maladies peuvent être responsables d’une augmentation de la production d’immunoglobulines. La distinction entre une augmentation polyclonale (plusieurs types d’immunoglobulines produites) et une augmentation monoclonale (un seul type d’immunoglobuline produite, traduisant une prolifération d’un seul clone de cellules lymphoïdes B fortement évocatrice d’une origine néoplasique) est indispensable pour préciser le diagnostic. Lorsque l’observation du tracé électrophorétique ne permet pas d’établir cette distinction, le recours à une immunoélectrophorèse, en identifiant les types d’immunoglobulines présentes dans le sérum, est nécessaire.

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9

Himberlin, C., B. Kolb, P. Delaby, A. M. Blaise, P. Y. Le Berruyer, S. Daliphard, and J. L. Pennaforte. "La lymphocytose polyclonale avec lymphocytes sanguins binucléés : Une entité à ne pas méconnaître." La Revue de Médecine Interne 23 (December 2002): 592s—593s. http://dx.doi.org/10.1016/s0248-8663(02)80478-7.

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10

Granel, B., P. Disdier, J. Serratrice, A. M. Hubert, M. C. Alessi, H. Cannoni, K. Mazodier, et al. "Hyperlymphocytose B polyclonale des tabagiques et anticorps antiphospholipides : à propos de trois cas." La Revue de Médecine Interne 21 (December 2000): 483. http://dx.doi.org/10.1016/s0248-8663(00)90042-0.

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11

Sebbar, J., F. Coutier, C. Golden, N. Razafindramaro, and C. Faure. "Hypergammaglobulinémie polyclonale en consultation de médecine interne : ne pas oublier l’endocardite à bartonelle !" La Revue de Médecine Interne 43 (December 2022): A457—A458. http://dx.doi.org/10.1016/j.revmed.2022.10.361.

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12

Grateau, G., C. Bachmeyer, O. Taulera, G. Sarfati, D. Séréni, B. Christoforov, and G. A. Cremer. "Fausses hyponatrémie et hyperphosphorémie au cours d'une infection par le virus VIH. Rôle de l'hypergammaglobulinémie polyclonale." La Revue de Médecine Interne 13, no. 6 (May 1992): S221. http://dx.doi.org/10.1016/s0248-8663(05)81693-5.

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13

Vignes, S., E. Oksenhendler, L. Quint, M. T. Daniel, X. Mariette, and J. P. Clauvel. "Hyperlymphocytose B polyclonale et hyper-lgM: déficit immunitaire et/ou prolifération lymphoïde bénigne associé(s) au tabac?" La Revue de Médecine Interne 20 (June 1999): s39. http://dx.doi.org/10.1016/s0248-8663(99)80144-1.

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Vignes, S., E. Oksenhendler, L. Quint, M. T. Daniel, X. Mariette, and J. P. Clauvel. "Hyperlymphocytose B polyclonale et hyper-IgM : déficit immunitaire et/ou prolifération lymphoïde bénigne associé(s) au tabac ?" La Revue de Médecine Interne 21, no. 3 (March 2000): 236–41. http://dx.doi.org/10.1016/s0248-8663(00)80042-9.

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15

Kündig, J., A. Keller, and C. Herbort. "Elévation polyclonale des immunoglofoulines: une aide plutôt qu'un piège dans le diagnostic des uvéites causées par la sarcoïdose." Klinische Monatsblätter für Augenheilkunde 204, no. 05 (May 1994): 323–29. http://dx.doi.org/10.1055/s-2008-1035549.

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16

Salih, Abdesslam, Abdelali El Kharrazi, Maria Lahlali, Asmae Lamine, Nada Lahmidani, Amine Mekkaoui, Mounia Elyousfi, et al. "PROFIL EPIDEMIOLOGIQUE, CLINICO-BIOLOGIQUE, THERAPEUTIQUE ET EVOLUTIF DES HEPATITES AUTO-IMMUNES (HAI) : A PROPOS DE 42 CAS." International Journal of Advanced Research 12, no. 09 (September 30, 2024): 1162–70. http://dx.doi.org/10.21474/ijar01/19549.

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Lhepatite auto-immune (HAI) est une maladie inflammatoire chronique du foie rare, tres heterogene, de cause inconnue. Lobjectif est de determiner le profil epidemiologique, clinico-biologique, therapeutique et evolutif des hepatites auto-immunes dans notre contexteÃ travers une etude retrospective descriptive realisee au sein du service de gastroenterologie du CHU de Fes incluant les patients atteints dune hepatite auto-immune colliges dans notre service entre janvier 2012 et juillet 2021. On a inclus 42 patients atteints dHAI. Le sex ratio homme (2) / (40) femme etait de 0,05 avec une moyenne dÃ¢ge de 51,04 (23-76). La maladie etait asymptomatique chez deux cas (4,7 %), dix cas (24%) admis sous forme dun tableau de decompensation dun foie de cirrhose, sept patients (16.6%)sous forme dune hepatite aiguÃ«. Par ailleurs, 23 cas (54,76 %) se sont presentes sous forme dune hepatite chronique. Les signes fonctionnels etaient domines par lasthenie chez 30 cas (71,42%). Le taux des transaminases (ASAT, ALAT) etait eleve chez 40 patients (95,2%), lEPP a objective une hypergammaglobulinemie polyclonale chez 29 cas (69%). Lechographie abdominale a objective unfoie dhepatopathie chronique avec signes dHTP chez 34 cas (81%), le bilan immunologique a objective des AAN positifs chez 19 patients, des Ac anti mitochondries chez 16 patients, des Anti-muscle lisse positifs chez 4 cas, des anti-SLA positifs chez 3 cas, Les moyens therapeutiques etaient domines par les corticoides, prescrits chez 100% des patients, suivis par lazathioprine chez 23 patients (54.7%). Une bonne reponse therapeutique a ete observee chez 71,4 % de nos patients, cinq cas ont rechute, cinq malades perdus de vue et 2 patientes decedees.

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17

Morizot, R., J. F. Lesesve, X. Troussard, and J. D. De Korwin. "Lymphocytose polyclonale à lymphocytes binucléés (LPLB) et critères du syndrome de fatigue chronique/intolérance systémique à l’effort : résultats d’une enquête auprès des patients du registre national des LPLB." La Revue de Médecine Interne 39 (June 2018): A104. http://dx.doi.org/10.1016/j.revmed.2018.03.350.

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18

Okada, H., Y. Shimabukuro, Y. Kassai, H. Ito, T. Matsuo, S. Ebisu, and Y. Harada. "The Function of Gingival Lymphocytes on the Establishment of Human Periodontitis." Advances in Dental Research 2, no. 2 (November 1988): 364–67. http://dx.doi.org/10.1177/08959374880020022801.

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Human periodontitis has been confirmed to be an IgG plasma cell-rich lesion. However, we also detected many T cells, both CD4-positive and CD8-positive cells, in periodontal lesions. Some of these T cells expressed HLA-DR (la-like) antigen on their surfaces, and the proportion of HLA-DR+ cells was approximately equal in both CD4+ and CD8+ cell populations (Okada et al., 1983, 1984). Consequently, both helper and suppressor T cells were believed to participate in the establishment of periodontal lesions. On the other hand, B cells were thought to be activated polyclonally in periodontal lesions, because a variety of periodontal florae possessed polyclonal B-cell-activating activity. We demonstrated that Actinomyces viscosus T14V stimulated mouse spleen B cells polyclonally and induced many IgM-producing cells but few IgG-producing cells. Moreover, IgG-producing cells were differentiated from only surface IgG-positive B cells but not from surface IgG-negative B cells-namely, surface IgM- or IgA-positive B cells (Harada et al., 1988). These results suggested that memory B cells, which had already been primed with appropriate antigens, might migrate into periodontal lesions, and then be activated polyclonally and develop into IgG-producing cells. The periodontal lesion could, therefore, be induced by the interactions of immunoregulatory mechanisms of T cells and polyclonal B cell activity of periodontal florae. In fact, L3T4-positive T cells (helper-inducer T cells) enhanced IgG synthesis of mouse spleen B cells which had been activated with T-independent B cell activators such as LPS and A. viscosus preparations (Okada et al., 1987; Ito et al., 1988). We hypothesized from the above results that autoreactive T cells recognized the increasing self-MHC class II(Ia) antigen on B cells which had been activated with polyclonal B cell activators, and then produced soluble factors, which could enhance IgG synthesis of these B cells. Autoreactive T cells as well as PBAs, thus, may play an important role in the establishment of the IgG plasma cell-rich periodontal lesion.

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19

Kapustianenko, L. G. "POLYCLONAL ANTIBODIES AGAINST HUMAN PLASMINOGEN KRINGLE 5." Biotechnologia Acta 10, no. 3 (June 2017): 41–49. http://dx.doi.org/10.15407/biotech10.03.041.

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20

Diall, O., V. M. Nantulya, Antony George Luckins, B. Diarra, and Boubacar Kouyaté. "Evaluation des tests immune-enzymatiques de détection des antigènes au moyen des anticorps mono- et polyclonaux pour le diagnostic de l’infection à Trypanosoma evansi chez le dromadaire (Camelus dromedarius)." Revue d’élevage et de médecine vétérinaire des pays tropicaux 45, no. 2 (February 1, 1992): 149–53. http://dx.doi.org/10.19182/remvt.8941.

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L'aptitude de deux tests ELISA d'absorption immuno-enzymatique utilisant, l'un un anticorps monoclonal spécifique anti-Trypanosoma brucei obtenu sur souris, l'autre des anticorps polyclonaux spécifiques de Trypanosoma evansi produits sur lapin, a été évaluée en vue de la détection des antigènes circulants comme méthode de diagnostic des infections à Trypanosoma evansi dans le sérum des dromadaires. Quatre vingt onze sérums d'un troupeau camelin témoin au Kenya indemne de T. evansi ont tous donné des résultats négatifs au test ELISA des anticorps monoclonaux et seuls deux d'entre eux (2,2 p. 100) ont donné des résultats faussement positifs avec les anticorps polyclonaux. Lors d'analyses ultérieures des sérums d'animaux infectés, les anticorps monoclonaux ont décelé les antigènes dans 90 sérums sur 108 testés (83,3 p. 100). Cette proportion s'est révélée inférieure pour les polyclonaux qui ont détecté les antigènes dans 67 des 110 sérums testés soit 60,9 p. 100. Dans une enquête portant sur 316 sérums provenant des régions de Gao et Nara au Mali, une forte proportion a réagi positivement aux antigènes (43,5 p. 100 pour le monoclonal et 42,9 p. 100 pour le polyclonal). Les tests ELISA se sont montrés au moins six fois plus sensibles que la technique de centrifugation de l'hématocrite.

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21

Yatsenko, T. A. "POLYCLONAL ANTIBODIES AGAINST HUMAN PLASMINOGEN: PURIFICATION, CHARACTERIZATION AND APPLICATION." Biotechnologia Acta 13, no. 6 (December 2020): 50–57. http://dx.doi.org/10.15407/biotech13.06.050.

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The plasminogen/plasmin system plays a crucial role in fibrinolysis and regulation of cell functions in a wide range of normal and pathological processes. Investigation of plasminogen/plasmin functions requires the availability of well-characterized and effective molecular tools, such as antibodies. In the present work, the isolation and characterization of rabbit polyclonal antibodies against human plasminogen are described and approaches for the identification of plasminogen and its fragments using the purified antibodies are demonstrated. For the antibodies isolation, standard animal immunization and blood collection procedures, serum isolation, protein salting out and affinity chromatography were performed. For the antibodies characterization and application, the following methods were used: enzyme linked immunoassay (ELISA), Western blotting, FITC-protein conjugation, flow cytometry and spectrofluorometry. The obtained polyclonal rabbit anti-human plasminogen antibodies interacted with human Glu- and Lys-plasminogen, kringles 1-3 and 1-4 of plasminogen, mini-plasminogen, the heavy and light chain of plasmin. We propose the application of anti-plasminogen antibodies for the direct ELISA, Western blot analysis, and for flow cytometry and spectrofluorometric analysis of plasminogen binding with cells. The obtained anti-plasminogen antibodies are promising tools for the investigation of plasminogen/plasmin system functions, either fibrinolytic or signaling.

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22

Gallacher, Gerard. "Polyclonal catalytic antibodies." Biochemical Society Transactions 21, no. 4 (November 1, 1993): 1087–90. http://dx.doi.org/10.1042/bst0211087.

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23

Van Wijngaerden, E., W. E. Peetermans, S. Van Lierde, and J. Van Eldere. "Polyclonal Staphylococcus Endocarditis." Clinical Infectious Diseases 25, no. 1 (July 1997): 69–71. http://dx.doi.org/10.1086/514499.

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24

Ostler, Elizabeth L., Marina Resmini, Keith Brocklehurst, and Gerard Gallacher. "Polyclonal catalytic antibodies." Journal of Immunological Methods 269, no. 1-2 (November 2002): 111–24. http://dx.doi.org/10.1016/s0022-1759(02)00228-4.

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25

Stephens, D. B., and B. L. Iverson. "Catalytic Polyclonal Antibodies." Biochemical and Biophysical Research Communications 192, no. 3 (May 1993): 1439–44. http://dx.doi.org/10.1006/bbrc.1993.1577.

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26

Tan, Kuan L., Peck L. Kiew, Nilanjon Naskar, and Jerry Y. Y. Heng. "A Novel Polyclonal Rabbit Immunoglobulin G Crystallisation Approach Using 3D Nanotemplate." International Journal of Chemical Engineering and Applications 7, no. 6 (December 2016): 369–72. http://dx.doi.org/10.18178/ijcea.2016.7.6.607.

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27

Norton, S. D., L. Zuckerman, K. B. Urdahl, R. Shefner, J. Miller, and M. K. Jenkins. "The CD28 ligand, B7, enhances IL-2 production by providing a costimulatory signal to T cells." Journal of Immunology 149, no. 5 (September 1, 1992): 1556–61. http://dx.doi.org/10.4049/jimmunol.149.5.1556.

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Abstract Previous studies demonstrated that a human pre-B acute lymphoblastic leukemia cell line, NALM-6, failed to stimulate a primary MLR, despite expression of class II MHC and adhesion molecules. Here we demonstrate that this is the result of the fact that NALM-6 cells do not express the ligand for CD28, namely B7. NALM-6 transfectants that expressed high levels of B7 gained the capacity to stimulate IL-2 production by class II MHC molecule-specific alloreactive T cells and to costimulate a polyclonal population of purified T cells cultured with immobilized anti-CD3 mAb. In the presence of PMA, NALM-6 cells transfected with B7 polyclonally stimulated T cells in a cyclosporine A-resistant fashion, a property previously attributed only to agonistic anti-CD28 mAb. The gain of these functions could not be explained solely by an increased capacity of the transfectants to form conjugates with T cells, suggesting that the CD28/B7 interaction transduces a costimulatory signal in T cells.

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28

Fu, Richard, Meghan J. Lyle, Xuefeng Wang, and Carol H. Miao. "Factor VIII-specific CAR regulatory T cells modulate murine anti-factor VIII immune responses." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 126.13. http://dx.doi.org/10.4049/jimmunol.196.supp.126.13.

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Abstract The immune response to factor VIII protein (FVIII; F8 in constructs) limits the effectiveness of treatments for hemophilia A (HemA) patients. Previously we demonstrated that regulatory T cells (Tregs) play a pivotal role in modulating anti-FVIII immune responses. For application of adoptive Treg therapy, we successfully expanded highly suppressive murine polyclonal Tregs antigen specifically in vitro. However, the FVIII-specific Tregs in the polyclonal population are still in very small numbers. Thus, we explored the strategy to generate FVIII-specific Tregs using the chimeric antigen receptor (CAR) approach. Lentiviral vector (LV) incorporating a high-binding anti-FVIII scFv linked to the CAR signaling domains and fused with a Foxp3 cDNA (F8CAR-Foxp3-LV) was prepared and used to transduce murine CD4+T cells. Flow cytometry analysis confirmed extracellular scFv and intracellular Foxp3 expression in transduced cells (F8CAR-Tregs). In vitro FVIII-specific suppressive assay showed that transduced cells had significantly higher suppressive activity than untransduced cells towards murine effector T cells. In addition, 1×106 transduced cells and untransduced cells were adoptively transferred into HemA mice and the treated mice were subsequently challenged with FVIII plasmid injected hydrodynamically. The anti-FVIII antibody titers are evaluated overtime. It is expected that F8CAR-Foxp3-LV transduced cells will prevent or decrease the production of anti-FVIII antibodies in HemA mice. We anticipate that compared with nonspecific or polyclonally expanded Tregs, FVIII-specific CAR Tregs will exert superior suppressive activity towards anti-FVIII immune responses without triggering systemic immune suppression.

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Mazov, A. V. ,. "GENERATION AND CHARACTERIZATION OF POLYCLONAL ANTIBODIES SPECIFIC TO HUMAN ESTROGEN RECEPTOR ERα." Biotechnologia Acta 17, no. 3 (June 28, 2024): 59–65. http://dx.doi.org/10.15407/biotech17.03.059.

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Aim. The purpose of the study was to generate and characterize anti-hERα polyclonal antibodies for elucidation of functional relationships between isoforms of estrogen receptor ERα and isoforms of ribosomal protein S6 kinase — S6K1. Methods. cDNA cloning. Expression of recombinant proteins in bacterial system. Affinity purification of His-tag fused recombinant proteins using Ni-NTA chromatography from bacterial lysates. Generation of polyclonal sera by mice immunization. Western blot analysis and immunoprecipitation. Results. cDNA coding for full length hERα was cloned into expression vector pET28a in frame with His-tag sequence. Recombinant hERα-His protein was expressed in E.Coli and purified by Ni-NTA chromatography. Purified hERα-His was used as antigen for mice immunization and generation of polyclonal antibodies. Specificity of polyclonal antibodies was analyzed by Western blot and immunoprecipitation of hERα from MCf-7 cell lysates. Conclusions. Generated anti-hERα polyclonal antibodies are of conformational type since specifically recognized hERα only in immunoprecipitation but not in Western blot. Created polyclonal antibodies a suitable for detection and analysis of hERα protein complexes.

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30

Hofer, Ursula. "Tracking down polyclonal tuberculosis." Nature Reviews Microbiology 19, no. 7 (May 20, 2021): 406. http://dx.doi.org/10.1038/s41579-021-00580-1.

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31

Fabijan, Aleksandra Petrovic, Nouri L. Ben Zakour, Josephine Ho, Ruby C. Y. Lin, and Jonathan Iredell. "Polyclonal Staphylococcus aureus Bacteremia." Annals of Internal Medicine 171, no. 12 (September 17, 2019): 940. http://dx.doi.org/10.7326/l19-0369.

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32

Ferrara, Fortunato, Sara D’Angelo, Tiziano Gaiotto, Leslie Naranjo, Hongzhao Tian, Susanne Gräslund, Elena Dobrovetsky, et al. "Recombinant renewable polyclonal antibodies." mAbs 7, no. 1 (January 2, 2015): 32–41. http://dx.doi.org/10.4161/19420862.2015.989047.

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33

Gavelli, Francesco, Ramona Bonometti, Mattia Bellan, Daniele Sola, Antonello Gibbin, Filippo Patrucco, Paolo Spina, et al. "Overlapping polyclonal lymphoproliferative disorders." National Medical Journal of India 33, no. 6 (2020): 344. http://dx.doi.org/10.4103/0970-258x.321144.

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34

STEPHENS, David B., Richard E. THOMAS, John F. STANTON, and Brent L. IVERSON. "Polyclonal antibody catalytic variability." Biochemical Journal 332, no. 1 (May 15, 1998): 127–34. http://dx.doi.org/10.1042/bj3320127.

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We have performed a systematic variability study of polyclonal antibody catalysis by using five rabbits immunized with the same hapten. Important results from this work are the following. (1) Similarities were observed in the catalytic polyclonal antibodies derived from all five rabbits. Four of the five rabbits produced polyclonal samples that were nearly the same in terms of catalytic activity, whereas the fifth rabbit, designated as rabbit 2, displayed a somewhat higher level of catalytic activity. The catalytic activities (as kcat/kuncat) of these polyclonal samples were similar to that from the best murine monoclonal antibody that had been previously elicited by the same hapten. (2) Titre was not an accurate indicator of polyclonal antibody catalytic activity. (3) A mathematical analysis to describe a distribution of Michaelis–Menten catalysts was performed to help interpret our results. (4) Kinetic analysis indicated that the binding parameters of the different samples were remarkably homogeneous, because one or two components were all that were required to fit the on-rate and off-rate data satisfactorily. Interestingly, the most active catalytic polyclonal sample, that from rabbit 2, displayed the slowest off-rate (so slow it could not be measured) and thus the highest overall affinity. (5) Catalytic analysis of eluted fractions of antibody from a substrate column indicated that each polyclonal sample was also relatively homogeneous in terms of catalytic parameters. The main conclusion of our study is that for this hapten–animal system, the overall catalytic immune response is relatively consistent at two levels. Consistent catalytic activity was observed between the polyclonal samples elicited in the different animals, and the elicited hapten-specific polyclonal antibodies were relatively homogeneous in terms of binding and catalytic parameters within each immunized animal. The observed similarities of the catalytic activity in the different animals is surprising, because the immune response is based on specific binding of antibodies to hapten. There is no known selective pressure to maintain consistent levels of catalytic activity. Our results can therefore be interpreted as providing evidence that for this hapten there is a fixed relationship between hapten structure and catalytic activity and/or consistent genetic factors that dominate the catalytic immune response.

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35

Troussard, X., H. Mossafa, and V. Salaün. "Persistant polyclonal lymphocytosis (PPLB)." Leukemia 13, no. 3 (March 1999): 497–98. http://dx.doi.org/10.1038/sj.leu.2401347.

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36

Maes, Bart D., and Yves F. Vanrenterghem. "Induction with polyclonal antibodies." Current Opinion in Organ Transplantation 4, no. 4 (December 1999): 305. http://dx.doi.org/10.1097/00075200-199912000-00002.

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37

BAUM, RUDY. "Polyclonal catalytic antibodies characterized." Chemical & Engineering News 71, no. 21 (May 24, 1993): 29–30. http://dx.doi.org/10.1021/cen-v071n021.p029.

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38

Brennan, D. C. "Polyclonal antibodies in immunosuppression." Transplantation Proceedings 33, no. 1-2 (February 2001): 1002–4. http://dx.doi.org/10.1016/s0041-1345(00)02304-6.

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39

Stephens, David B., Britta H. Wilmore, and Brent L. Iverson. "Polyclonal antibodies and catalysis." Bioorganic & Medicinal Chemistry 2, no. 7 (July 1994): 653–58. http://dx.doi.org/10.1016/0968-0896(94)85014-3.

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40

van Engelen, Baziel G. M., David J. Miller, and Moses Rodriguez. "Polyclonal Ig: an immunopharmacon?" Immunology Today 15, no. 7 (July 1994): 341–42. http://dx.doi.org/10.1016/0167-5699(94)90085-x.

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41

Monti, Simona M., Vincenzo Fogliano, Giacomino Randazzo, Giuseppe Peluso, Antonio Logrieco, and Alberto Ritieni. "Polyclonal antibodies against fusaproliferin." Canadian Journal of Microbiology 45, no. 1 (January 1, 1999): 45–50. http://dx.doi.org/10.1139/w98-116.

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Fusaproliferin (FP), a toxic metabolite of the world-wide maize pathogens Fusarium proliferatum and Fusarium subglutinans, was recently found to be a natural contaminant of maize. Its toxic activity on haematopoietic human cell lines and its teratogenic effects on chicken embryos has been recently proved. Therefore a sensitive, rapid, and inexpensive screening test to detect FP in agricultural commodities is necessary to protect human health. FP-hemiglutarate conjugated to modified bovine serum albumin was synthesized, characterized, and used as an antigen for raising polyclonal antibodies by immunizing rabbits. Indirect and competitive ELISA and immunoblotting analyses were performed to determine antibody specificity towards the mycotoxin. The determination of 10 µg of free FP/mL was achieved using antibodies purified by means of affinity chromatography on a FP-lysine-Sepharose column. This unsatisfactory detection limit is due to high background values; thus, this method is not competitive with traditional UV-HPLC methods.Key words: fusaproliferin, ELISA, mycotoxin, immunoassay, corn, Fusarium.

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42

Forsythe, John L. R. "ATG- a polyclonal sledgehammer?" Transplant Immunology 2, no. 2 (June 1994): 148–52. http://dx.doi.org/10.1016/0966-3274(94)90049-3.

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43

Deplano, Simona, Elizabet Nadal-Melsió, and Barbara J. Bain. "Persistent polyclonal B lymphocytosis." American Journal of Hematology 89, no. 2 (February 2014): 224. http://dx.doi.org/10.1002/ajh.23630.

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44

Rodríguez, J. N., J. C. Diéguez, M. L. Martino, D. Prados, and D. M. Aguayo. "Persistent polyclonal B lymphocytosis." American Journal of Hematology 51, no. 3 (March 1996): 246–47. http://dx.doi.org/10.1002/(sici)1096-8652(199603)51:3<246::aid-ajh15>3.0.co;2-e.

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45

Cooper, Helen M., and Yvonne Paterson. "Production of Polyclonal Antisera." Current Protocols in Neuroscience 00, no. 1 (September 1997): 5.5.1–5.5.9. http://dx.doi.org/10.1002/0471142301.ns0505s00.

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Peterson, Loann C., Brian Kueck, Diane C. Arthur, Kenneth Dedeker, and Richard D. Brunning. "Systemic polyclonal immunoblastic proliferations." Cancer 61, no. 7 (April 1, 1988): 1350–58. http://dx.doi.org/10.1002/1097-0142(19880401)61:7<1350::aid-cncr2820610713>3.0.co;2-u.

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47

van Kamp, H., WE Fibbe, RP Jansen, M. van der Keur, E. de Graaff, R. Willemze, and JE Landegent. "Clonal involvement of granulocytes and monocytes, but not of T and B lymphocytes and natural killer cells in patients with myelodysplasia: analysis by X-linked restriction fragment length polymorphisms and polymerase chain reaction of the phosphoglycerate kinase gene." Blood 80, no. 7 (October 1, 1992): 1774–80. http://dx.doi.org/10.1182/blood.v80.7.1774.1774.

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Abstract To determine the clonal nature of hematopoiesis and to assess lineage involvement in patients with myelodysplastic syndromes (MDS), we used restriction fragment length polymorphisms of the X-linked genes phosphoglycerate kinase (PGK1) and hypoxanthine phosphoribosyltransferase (HPRT) and the X-linked probe M27 beta. Eleven female MDS patients heterozygous for at least one of these probes were studied: 3 with refractory anemia (RA), 2 with RA with ringed sideroblasts (RARS), 2 with chronic myelomonocytic leukemia (CMML), and 4 with RA with excess of blasts in transformation (RAEB-t). All exhibited clonal hematopoiesis as determined by Southern analysis of DNA prepared from peripheral blood (PB) and/or bone marrow (BM) cells. In three of the six patients heterozygous for the PGK1 gene, purified cell suspensions of polymorphonuclear cells (PMN), monocytes, lymphocytes, and/or T cells prepared from PB were tested. In addition, five of these patients were analyzed by a polymerase chain reaction (PCR)-based procedure as described recently. This method was slightly adapted to facilitate the analysis of cell lysates of fluorescence- activated cell sorted (FACS) monocytes, T and B lymphocytes, and natural killer (NK) cells. The outcome of Southern and PCR analysis was concordant, showing that PMN and monocytes were clonally derived, whereas circulating T and B lymphocytes and NK cells exhibited random X- chromosome inactivation compatible with a polyclonal pattern. To address the question of whether T cells are derived from unaffected progenitor cells or that their origin had antedated the onset of MDS, naive and memory T cells were analyzed separately. Both subsets showed a polyclonal pattern. However, in one patient analysis of constitutive DNA suggested a skewed methylation, and the presence of clonal lymphocytes against a background of polyclonal lymphoid cells cannot be ruled out in this patient. PCR analysis of PB and BM cells showed a nonrandom, unilateral pattern of X-inactivation, compatible with a mixture of clonally (myeloid) and polyclonally (lymphoid) derived cells. In conclusion, in some patients, MDS represents a disorder with clonal hematopoiesis restricted to cells of myeloid origin, whereas a random X-inactivation pattern is found in lymphoid cells.

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48

van Kamp, H., WE Fibbe, RP Jansen, M. van der Keur, E. de Graaff, R. Willemze, and JE Landegent. "Clonal involvement of granulocytes and monocytes, but not of T and B lymphocytes and natural killer cells in patients with myelodysplasia: analysis by X-linked restriction fragment length polymorphisms and polymerase chain reaction of the phosphoglycerate kinase gene." Blood 80, no. 7 (October 1, 1992): 1774–80. http://dx.doi.org/10.1182/blood.v80.7.1774.bloodjournal8071774.

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Abstract:

To determine the clonal nature of hematopoiesis and to assess lineage involvement in patients with myelodysplastic syndromes (MDS), we used restriction fragment length polymorphisms of the X-linked genes phosphoglycerate kinase (PGK1) and hypoxanthine phosphoribosyltransferase (HPRT) and the X-linked probe M27 beta. Eleven female MDS patients heterozygous for at least one of these probes were studied: 3 with refractory anemia (RA), 2 with RA with ringed sideroblasts (RARS), 2 with chronic myelomonocytic leukemia (CMML), and 4 with RA with excess of blasts in transformation (RAEB-t). All exhibited clonal hematopoiesis as determined by Southern analysis of DNA prepared from peripheral blood (PB) and/or bone marrow (BM) cells. In three of the six patients heterozygous for the PGK1 gene, purified cell suspensions of polymorphonuclear cells (PMN), monocytes, lymphocytes, and/or T cells prepared from PB were tested. In addition, five of these patients were analyzed by a polymerase chain reaction (PCR)-based procedure as described recently. This method was slightly adapted to facilitate the analysis of cell lysates of fluorescence- activated cell sorted (FACS) monocytes, T and B lymphocytes, and natural killer (NK) cells. The outcome of Southern and PCR analysis was concordant, showing that PMN and monocytes were clonally derived, whereas circulating T and B lymphocytes and NK cells exhibited random X- chromosome inactivation compatible with a polyclonal pattern. To address the question of whether T cells are derived from unaffected progenitor cells or that their origin had antedated the onset of MDS, naive and memory T cells were analyzed separately. Both subsets showed a polyclonal pattern. However, in one patient analysis of constitutive DNA suggested a skewed methylation, and the presence of clonal lymphocytes against a background of polyclonal lymphoid cells cannot be ruled out in this patient. PCR analysis of PB and BM cells showed a nonrandom, unilateral pattern of X-inactivation, compatible with a mixture of clonally (myeloid) and polyclonally (lymphoid) derived cells. In conclusion, in some patients, MDS represents a disorder with clonal hematopoiesis restricted to cells of myeloid origin, whereas a random X-inactivation pattern is found in lymphoid cells.

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Kokošková, B., I. Pánková, and V. Krejzar. "Characteristics of polyclonal antisera for detection and determination of Clavibacter michiganensis subsp. insidiosus." Plant Protection Science 36, No. 2 (January 1, 2000): 46–52. http://dx.doi.org/10.17221/9621-pps.

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50

Käfer, Rudolf, Lisa Schmidtke, Katharina Schrick, Evelyn Montermann, Matthias Bros, Hartmut Kleinert, and Andrea Pautz. "The RNA-Binding Protein KSRP Modulates Cytokine Expression of CD4+ T Cells." Journal of Immunology Research 2019 (August 14, 2019): 1–15. http://dx.doi.org/10.1155/2019/4726532.

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The KH-type splicing regulatory protein (KSRP) is a RNA-binding protein, which regulates the stability of many mRNAs encoding immune-relevant proteins. As KSRP regulates innate immune responses, for instance by the modulation of type I interferon mRNA stability, we were interested whether knockdown of the protein (KSRP-/-) interferes with T cell activation and polarization. Polyclonally stimulated KSRP-/- CD4+ T cells proliferated at a higher extent and higher frequency and expressed the activation marker CD25 more than wild-type T cells. In supernatants of stimulated KSRP-/- CD4+ T cells, levels of IL-5, IL-9, IL-10, and IL-13 were observed to be increased compared to those of the control group. KSRP-/- CD8+ T cells showed no altered proliferative capacity upon polyclonal stimulation, but supernatants contained lower levels of interferon-γ. Similar changes in the cytokine expression patterns were also detected in T cells derived from KSRP-/- mice undergoing arthritis induction indicative of a pathophysiological role of KSRP-dependent T cell polarization. We demonstrated the direct binding of KSRP to the 3′ untranslated region of IL-13, IL-10, and IFN-γ mRNA in in vitro experiments. Moreover, since IL-4 mRNA decay was reduced in KSRP-/- CD4+ T cells, we identify KSRP as a negative regulator of IL-4 expression. These data indicate that overexpression of IL-4, which constitutes the primary inducer of Th2 polarization, may cause the Th2 bias of polyclonally stimulated KSRP-/- CD4+ T cells. This is the first report demonstrating that KSRP is involved in the regulation of T cell responses. We present strong evidence that T cells derived from KSRP-/- mice favor Th2-driven immune responses.

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