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Advances in Immunology Volume 108 1st Edition
Frederick W. Alt (Ed.) Digital Instant Download
Author(s): Frederick W. Alt (ed.), K. Frank Austen (ed.), Tasuku Honjo (ed.),
Fritz Melchers (ed.), Jonathan W. Uhr (ed.), Emil R. Unanue (ed.)
ISBN(s): 9780123809957, 0123809959
Edition: 1st
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Year: 2010
Language: english

Advances in
IMMUNOLOGY
VOLUME
108

This page intentionally left blank

Advances in
IMMUNOLOGY
VOLUME
108
Edited by
FREDERICK W. ALT
Howard Hughes Medical Institute, Boston,
Massachusetts, USA
Associate Editors
K. FRANK AUSTEN
Harvard Medical School, Boston, Massachusetts, USA
TASUKU HONJO
Kyoto University, Kyoto, Japan
FRITZ MELCHERS
University of Basel, Basel, Switzerland
JONATHAN W. UHR
University of Texas, Dallas, Texas, USA
EMIL R. UNANUE
Washington University, St. Louis, Missouri, USA
AMSTERDAM • BOSTON • HEIDELBERG • LONDON
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ISSN: 0065-2776 (series)
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10 11 10 9 8 7 6 5 4 3 2 1

CONTENTS
Contributors vii
1. Macrophage Proinflammatory Activation and Deactivation:
A Question of Balance 1
Annabel F. Valledor, Monica Comalada, Luis Santamarı́a-Babi,
Jorge Lloberas, and Antonio Celada
1. Introduction 3
2. The Two Faces of Inflammation 4
3. Macrophage Proinflammatory Activities 5
4. Macrophage Deactivation 7
5. Concluding Remarks 16
Acknowledgment 16
References 16
2. Natural Helper Cells: A New Player in the Innate Immune
Response against Helminth Infection 21
Shigeo Koyasu, Kazuyo Moro, Masanobu Tanabe,
and Tsutomu Takeuchi
1. Introduction: Helminth Infection and Th2 Immunity 22
2. Helminths’ Invasion and Host Immune Responses 23
3. Induction of Th2 Immune Responses 27
4. Th2-Inducing Cytokines in Innate Immune Phases 29
5. Cells Producing Th2 Cytokines in Innate Immune Responses 31
6. Perspectives 36
Acknowledgments 37
References 37
3. Mapping of Switch Recombination Junctions, a Tool for Studying
DNA Repair Pathways during Immunoglobulin Class Switching 45
Janet Stavnezer, Andrea Björkman, Likun Du, Alberto Cagigi,
and Qiang Pan-Hammarström
1. Introduction to Class Switch Recombination 47
2. Characteristics of S–S Recombination Junctions 53
3. Effect of DNA Repair Deficiencies on S–S Junctions 73
v

4. Discussion 95
Acknowledgments 100
References 101
4. How Tolerogenic Dendritic Cells Induce Regulatory T Cells 111
Roberto A. Maldonado and Ulrich H. von Andrian
1. Introduction 112
2. What is the Origin of Treg-Inducing tDCs? 118
3. Instructive Signals for Treg-Inducing tDCs 128
4. How are tDCs Inducing Tregs? 139
Acknowledgments 144
References 144
Index 167
Contents of Recent Volumes 171
vi Contents

CONTRIBUTORS
Numbers in parentheses indicate the pages on which the authors’ contributions begin.
Andrea Björkman
Division of Clinical Immunology, Department of Laboratory Medicine,
Karolinska Institutet at Karolinska University Hospital Huddinge,
Stockholm, Sweden (45)
Alberto Cagigi
Antonio Celada
Macrophage Biology Group, Institute for Research in Biomedicine, (IRB
Barcelona), and University of Barcelona, Barcelona, Spain (1)
Monica Comalada
Likun Du
Shigeo Koyasu
Department of Microbiology and Immunology, Keio University School of
Medicine, Tokyo, Japan (21)
Jorge Lloberas
Roberto A. Maldonado
Department of Pathology, Harvard Medical School, Boston,
Massachusetts, USA (111)
vii

Kazuyo Moro
Department of Microbiology and Immunology, Keio University School of
Medicine, Tokyo, Japan (21)
Qiang Pan-Hammarström
Luis F. Santamarı́a-Babi
Janet Stavnezer
Department of Microbiology and Physiological Systems, Program in
Immunology and Virology, University of Massachusetts Medical School,
Worcester, Massachusetts, USA (45)
Tsutomu Takeuchi
Department of Parasitology and Tropical Medicine, Keio University
School of Medicine, Tokyo, Japan (21)
Masanobu Tanabe
Department of Parasitology and Tropical Medicine, Keio University
School of Medicine, Tokyo, Japan (21)
Annabel F. Valledor
Nuclear Receptors Group, Department of Physiology, School of Biology,
Barcelona, Spain (1)
Ulrich H. von Andrian
Department of Pathology, and Immune Disease Institute, Harvard
Medical School, Boston, Massachusetts, USA (111)
viii Contributors

CHAPTER 1
Macrophage Proinflammatory
Activation and Deactivation:
A Question of Balance
Annabel F. Valledor,* Monica Comalada,†
Luis F. Santamarı́a-Babi,†
Jorge Lloberas,†
and
Antonio Celada†
Contents 1. Introduction 3
2. The Two Faces of Inflammation 4
3. Macrophage Proinflammatory Activities 5
3.1. IFN-g 5
3.2. LPS 6
4. Macrophage Deactivation 7
4.1. Signal-specific mechanisms 8
4.2. Gene-specific mechanisms 12
4.3. Cytokines 14
4.4. Nuclear receptors 14
Acknowledgment 16
References 16
Abstract Macrophages play key roles in inflammation. During the onset of
the inflammatory process, these phagocytic cells become activated
and have destructive effects. Macrophage activation, which
involves the induction of more than 400 genes, results in an
increased capacity to eliminate bacteria and to regulate many
other cells through the release of cytokines and chemokines.
Advances in Immunology, Volume 108 # 2010 Elsevier Inc.
ISSN 0065-2776, DOI: 10.1016/S0065-2776(10)08001-6 All rights reserved.
* Nuclear Receptors Group, Department of Physiology, School of Biology, Barcelona, Spain
{
Macrophage Biology Group, Institute for Research in Biomedicine, (IRB Barcelona), and University of
Barcelona, Barcelona, Spain
1

However, excessive activation has damaging effects, such as septic
shock, which can lead to multiple organ dysfunction syndrome and
death. In other situations, persistence of proinflammatory activity
results in the development of chronic inflammation, such as rheu-
matoid arthritis, psoriasis, and inflammatory bowel disease. To
prevent undesirable effects, several mechanisms have evolved to
control the excess of activation, thereby leading to macrophage
deactivation and the resolution of inflammation. In this review, we
discuss several mechanisms that mediate macrophage deactivation.
ABBREVIATIONS
ATF2 activating transcription factor 2
BCL-3 B cell lymphoma 3
CBP CREB-binding protein
C/EBPd CCAAT/enhancer-binding protein-d
CIS cytokine inducible SH2-containing protein
COX-2 cyclooxygenase-2
CREB1 cAMP-responsive-element-binding protein 1
DCs dendritic cells
DUSP1 dual specificity phosphatase 1
ERK external regulated kinase
GR glucocorticoid receptor
HATs histone acetyltransferases
HDACs histone deacetylases
Hes hairy and enhancer of split
Hey hairy/enhancer-of-split related with YRPW motif
IFN-g interferon-gamma
IkB inhibitor of nuclear factor kappaB
IRFs IFN-regulatory factors
IL interleukin
IL1Rl1L/ST2L IL-1 receptor-like 1 ligand
IRAKM IL-1 receptor-associated kinase M
JAK janus kinase
LBP lipoprotein binding protein
LPS lipopolysaccharide
JNK-1 junk N-terminal kinase
LXR liver X receptor
MAPK mitogen-activated protein kinase
MKP-1 phosphatase 1 of MAPK
MyD88 myeloid differentiation primary response gene 88
MyD88(S) myeloid differentiation primary response gene 88
(short isoform)
2 Annabel F. Valledor et al.

NAD nicotinamide adenine dinucleotide
NO nitric oxide
NOS2 nitric oxide synthase 2
PIAS protein inhibitor of activated STAT
PKA protein kinase A
PMNs polymorphonuclear neutrophils
PPAR peroxisome proliferator-activated receptor
PTEN phosphatase and tensin homolog deleted on
chromosome ten
PTP1B protein tyrosine phosphatase 1B
RUNX1 runt-related transcription factor 1
SHIP SH2-containing 50
-inositol phosphatase
SHP-1 SH2-containing phosphatase 1
SIRT sirtuin
SOCS suppressors of cytokine signaling
STAT signal transducer and activator of transcription
sTLR4 soluble TLR4
SUMO small ubiquitin-related modifier
TOLLIP toll-interacting protein
TGFb transforming growth factor-beta
TLR-4 toll-like receptor 4
TNF-a tumor necrosis factor-alpha.
1. INTRODUCTION
When a microorganism enters the body and remains at a local site, a
reaction is initiated in order to remove or inactivate the nonself element
and to repair the damage caused by this reaction. This process is called
inflammation and it has been recognized by its cardinal signs (heat,
redness, swelling, and pain) since the early days of medicine. Inflamma-
tion is induced by changes in the microcirculation that allow large
amounts of serum proteins and leukocytes to move from the blood to
the affected tissue.
The first cells that selectively distinguish between self- and nonself
elements at the inflammatory loci are innate-type lymphocytes, including
B1, natural killer cells, and g/d T lymphocytes. They recognize danger-
and pathogen-associated molecular patterns and respond to them by
producing cytokines. The type of cytokines released during these early
stages depends on the invading microorganism and influences the nature
of the subsequent immune response (Th1, Th2, or Th17 response). The
first cells to move from the blood to the inflammatory site are Ly6C
monocytes, which secrete a number of chemokines that attract polymor-
phonuclear neutrophils (PMNs) (Auffray et al., 2007). During the first
Macrophage Proinflammatory Activation and Deactivation: A Question of Balance 3

hours of infection, PMNs massively enter the site of inflammation, fol-
lowed by Ly6Cþ
monocytes 24 h later. The differential time-course in the
recruitment of PMNs and Ly6Cþ
monocytes has been associated with the
expression of selective chemokines and leukocyte-endothelial adhesion
molecules. The initial goal of these phagocytic cells is to kill and eliminate
the invading microorganisms (proinflammatory activity). During this
process, most of the neutrophils die by apoptosis. Once the injurious
stimulus is cleared, healthy tissue structure and function is restored
(anti-inflammatory activity). Depending on the amount of time required
to remove the harmful agent, activation of the acquired immune system
may also take place. Although the cardinal signs of inflammation have
been known for a long time, the mechanisms and mediators involved in
this process have been largely ignored and have only recently begun to be
elucidated.
2. THE TWO FACES OF INFLAMMATION
The goal of the inflammatory process is to remove noxious agents, thus
protecting the body against infection. In the early stage of inflammation,
neutrophils kill microorganisms very efficiently. Soon after entering tis-
sues, neutrophils promote the switch of arachidonic acid-derived prosta-
glandins and leukotrienes to lipoxins, which inhibit further neutrophil
recruitment and trigger neutrophil apoptosis within the inflammatory
site (Serhan and Savill, 2005). The remaining microorganisms are then
eliminated by infiltrating macrophages. For this purpose, macrophages
use several potent mechanisms, including the production of reactive
oxygen species (ROS), nitric oxide (NO), and the release of several
enzymes and cytokines, including tumor necrosis factor-alpha (TNF-a),
interleukin-1beta (IL-1b), IL-6, etc. The duration of this proinflammatory
phase depends on the balance between the capacity of the microorganisms
to survive and the capacity of the macrophages to remove them. If during
this period macrophages are able to control the infection and eliminate the
pathogen, then a second phase is initiated in which macrophages exert
anti-inflammatory activity. The release of anti-inflammatory and reparative
cytokines such as transforming growth factor-beta (TGF-b) and recently
identified lipid mediators such as lipoxins, resolvins, and protectins pre-
dominate during this phase. Resolvins and protectins are oxygenation
products derived from omega-3 polyunsaturated fatty acids, which,
together with lipoxins, act coordinately to suppress local inflammatory
cell influx and enhance the clearance of apoptotic bodies (Kohli and
Levy, 2009). The objective is now to repair the damage produced during
the proinflammatory phase, similarly to a process of wound healing, thus
4 Annabel F. Valledor et al.

leading to the resolution of inflammation. The anti-inflammatory program
ends with the departure of macrophages through the lymph.
Under normal circumstances in which macrophages kill or inactivate
microorganisms through the development of a granuloma, the phases of
destruction and repair are well balanced. However, under persistence of
the proinflammatory phase or when macrophages trigger an altered
response, acute infection may result in chronic inflammation (Kim et al.,
2008). An excess of activation, for example, as a response to circulating
lipopolysaccharide (LPS), may lead to sepsis and subsequent septic shock.
To limit inflammation-associated pathology, the cells become hypore-
sponsive to LPS (tolerance to LPS) during conditions of excessive inflam-
mation. LPS-tolerant cells are refractory to the induction of inflammatory
cytokines such as TNF-a and IL-6, and this is due, at least in part, to the
downregulation of several inflammatory signaling molecules (Foster and
Medzhitov, 2009). In an experimental model of arthritis, the signature of
oxidative metabolism and the mode of macrophage activation determine
the shift from acute to chronic disease (Takahashi et al., 2008). Failure to
resolve inflammation is also a key event in atherosclerosis (Tabas, 2010).
On the other end of the spectrum, an excess of anti-inflammatory activity
can result in progressive fibrosis (Wynn, 2008). Therefore, the activity of
macrophages in both the proinflammatory and the resolution phases is
complex and must be tightly regulated.
3. MACROPHAGE PROINFLAMMATORY ACTIVITIES
3.1. IFN-g
In order to become activated and fully functional, macrophages at the
inflammatory site must interact with a variety of Th1-type cytokines, such
as interferon-gamma (IFN-g). Upon recognition of IFN-g, its specific
receptor triggers the sequential activation of the Janus kinase (JAK)-signal
transducer and activator of transcription (STAT) pathway, which results
in transcriptional upregulation of more than 400 genes (Bach et al., 1997;
Billiau and Matthys, 2009; Stark, 2007). Many IFN-g-induced functions are
mediated by direct activation of immune effector genes by STAT1, includ-
ing genes encoding antiviral proteins, microbicidal molecules, phagocytic
receptors, chemokines, cytokines, and antigen-presenting molecules.
There is accumulating evidence that cytoplasmic inactive STAT1 is pres-
ent predominantly as unphosphorylated homodimers in an equilibrated
state between a parallel and an antiparallel configuration (Ota et al., 2004).
After interaction of IFN-g with the corresponding receptor, a signaling is
produced inducing JAKs to phosphorylate STAT1 on tyrosine 701. This
produces a dimer configuration of STAT1 and the nuclear translocation
Macrophage Proinflammatory Activation and Deactivation: A Question of Balance 5

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*** START OF THE PROJECT GUTENBERG EBOOK PETIT HISTOIRE
DES GRANDES ROIS DE ANGLETERRE ***

Note sur la transcription: Les erreurs clairement
introduites par le typographe ont été corrigées.
L'orthographe d'origine a été conservée et n'a pas été
harmonisée. Les numéros des pages blanches n'ont pas
été repris.
Les autres erreurs très apparentes (mots masculins en
féminin et/ou le contraire), sont voulues par l'auteur. Il
paraît qu'il s'agit de l'humour typiquement québécois.
Petit Histoire des Grandes
Rois
de Angleterre

Petit Histoire
DES
Grandes Rois
DE
Angleterre
PAR
OUN COLONISTE DES PLUS VERIDIQUES
Edition augmentée,
agrandie et beaucoup additionnée
QUEBEC
Typ. Laflamme Proulx
1910

AVERTISSEMENT
L y a quelques années, un ami des Canadiens-français,
feu M. le docteur W.-H. Drummond, de Montréal, prenait
plaisir à publier, de temps à autre, dans les journaux de
la métropole, des pièces rimées au cours desquelles il
prêtait à de nos compatriotes français un langage formé
d'un mélange d'expressions anglaises apprises, pour ainsi dire, à la
volée, et de tournures françaises d'une saveur de terroir des plus
prononcées. Ce rapprochement à la bonne franquette des deux
idiomes de notre pays amenait, va sans dire, des situations d'un
réalisme amusant, bien que parfois poussé à des limites
invraisemblables. Je n'en veux donner pour exemple que les
quelques vers suivants, que je tire du volume intitulé The Habitant,
dans lequel le poète anglais a réuni ses pièces:
I read on de paper
mos' ev'ry day all about Jubilee
An' grande procession movin' along, an' across de sea,
Dat's children of Queen Victoriaw comin' from far away
For tole Madame w'at dey think of her, an' wishin' her
bonne santé.
An' if anyman want to know pourquoi les Canayens
should be dere
Wit' res of de worl' for shout Hooraw an' t'row hees
cap on de air,
Purty quick I will tole heem the reason w'y we feel lak'
de oder do.

For if I'm only poor habitant I'm not on de sapré fou.
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
. . .
So de sam' as two broder we settle down, leevin' dere
han' in han',
Knowin' each oder, we lak' each oder, de French an' de
Englishman,
For it's curi's t'ing on dis worl', I'm sure you see it agen
an agen
Dat offen de mos' worse ennemi, he's comin' de bes',
bes' friend.
J'eus dans le temps,—c'était en 1897,—l'idée de répondre au
badinage du sympathique docteur en faisant, à mon tour, parler en
français un de nos compatriotes anglais; et c'est alors que parut
dans certains journaux de Québec et de Montréal une pièce que
j'avais intitulée: Ode à Victoria Ire à l'occasion qu'elle joubile en
Diamond. L'accueil bienveillant qui lui fut fait m'engagea, un peu
plus tard, à écrire la Petit Histoire dont je me permets de présenter
aujourd'hui l'édition «augmentée, agrandie et beaucoup
additionnée». Puisse-t-elle être accueillie par nos compatriotes de
langue anglaise avec le même esprit de bienveillance que nous
apportons encore nous-mêmes à la lecture du livre humoristique de
M. le docteur Drummond.
Nous vivons dans un pays où la connaissance des langues anglaise
et française est non seulement utile, mais d'une nécessité de tous
les instants. Chacun de nous sait bien—disons-le toujours!—
s'exprimer d'une manière passable dans sa langue maternelle; mais,
lorsque nous nous trouvons aux prises avec l'autre langue, celle qui
nous est moins familière, nous sommes plus ou moins portés à
commettre des hérésies ou d'amusants quiproquos qu'un peu de
réflexion, suggérée peut-être par la critique, pourrait nous faire
éviter.

C'est sans doute dans cet esprit que le docteur Drummond a écrit
ses poèmes humoristiques, et c'est pareillement, que l'on veuille
bien le croire, sans plus de méchanceté que je mets ma Petit
Histoire sous les yeux des lecteurs anglais. On réussit parfois à faire,
au moyen d'un simple badinage de bon aloi, ce que ne saurait
accomplir une démonstration sérieuse et compliquée.
Ephrem Chouinard

AVANT-PROPOS
Pour bien comprenner le Histoire
De ce qu'on appelle les rois,
Il faut fixer dans son mémoire
Certains points au nombre de trois,
Savoir: tout d'abord la première;
Ensouite la numero deux;
Puis, enfin, vienné le dernière
Qui n'est pas la moindre d'entr'eux.
La roi, qu'il soit mâle ou femelle,
Est oun être qui vient d'En Haut,
Et, par conséquent, tout en elle
Doit être trouvé bonne et beau.
C'est la premier point. La deuxième,
Venant ensouite du premier,
C'est que, pour oun roi vilain même,
Chacun doit être coutumier
D'aller se jeter dans le braise
Pour y rester tant qu'il est cuit,
Et se considérer fort aise
De s'être fait griller pour lui.
La troisième est beaucoup curieuse:
C'est que la roi «can do no wrong»,
Que ce soit dans le guerre affreuse
Ou la simple jeu de Ping-Pong.
Bien! En mettant dans votre tête
Ces trois points dextrement trouvés,
Vous ne jugerez rien de bête
Dans les faits qui sont relevés,

Sur la trône de Angleterre
On vit si tant de grandes rois
Qu'on ne savé plus comment faire
Pour le dire assez bien des fois.
Depouis la tout premier d'entr'elles
Jousqu'à notre saige Edouard Sept,
Tous nos monarques sontaient belles
Et beaucoup grands, comme l'on sait.
Dans les autres pays du monde
Oh! l'on vit bien, de temps en temps,
Certains rois de savoir profonde
Ou possédant d'autres talents.
Mais ce n'était point le coutume
Et, je le dis en vérité,
Trop souvent la royal costume
Cachait le médiocrité.
Bien, chez nous c'été différente;
De rois savants et pleins d'honneur
Nous avons eu souite charmante
Et tout ce qui fut la meilleur.
Quant aux monarques féminines,
C'était aussi pareil toujiours,
Et de plus vertueuses mines
Jamais vit-on meilleur concours.
Je ne dis pas que rois et reines
N'eurent jamais de manquements,
Ni que souvent par grandes haines
Ils n'ont pas fait souffrir leurs gens.
D'aucuns ont commis des sottises,
Volé les biens de leurs voisins,
Pillé les trésors des églises
Et dans la sang trempé leurs mains.
Quelques-uns ont battu leurs mères,
Assassiné frères et sœurs;
Mais, à part ces petits misères,
Oh! c'était d'excellentes cœurs.

Je veux vous en donner les preuves
Par cette histoire en raccourci
Que, dans ces vers tout à fait neuves,
Je vais vous présenter ici.
Race Saxonne

EGBERT-LE-GRAND
(827-837)
Oun roi sauvaige ou chef de bande
Etait Egbert probablement,
Et qu'il était d'oun vertu grande
Nul n'affirmerait sous serment.
Issu de le race saxonne,
Il été la premier garçon
Qui porta l'anglaise couronne
D'oune indépendante façon.
On ne sait pas de lui grand chose,
Ni s'il fut bon, nul ou méchant;
Et, peut-être pour cette cause,
On le surnomme Egbert-le-Grand.
Peut-être aussi cet nom splendide
Lui vienné de ce qu'oun beau jour
En France d'oun pas très rapide
Il dut aller faire oun séjour;

Et ce fut la roi Charlemagne
Qui le reçut dans sa palais [1].
Chacun sait que toujours on gagne
A fréquenter les gens replets.
Le puce qui pique oun princesse,
Par exemple, il est plus heureux
Qu'oun pauvre ciron en détresse,
Dessus le peau d'oun miséreux.
Charlemagne étant maggnifique,
Egbert fit bien de frotter lui;
Et c'est oun saige politique
Qui soubsisté même aujourd'hui.
Que d'êtres d'insiggnificance
Atteignent la plus haut crédit,
Pour avoir avec persistance
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[1] Voir note à l'appendice.

ETHELWOLF 836-858
ETHELBALD 858-860
ETHELBERT 860-866
ETHELRED Ier 866-871
Puis, pour trente ans le Angleterre
Fut en guerre avec les Danois
Qui les Anglais mettaient à terre
Souvent et beaucoup à le fois.
Cependant l'anglaise couronne
Il ne fut pas foulée aux pieds,
Mais retomba sur le personne
De rois plus ou moins estropiés.
Ethelwolf il vint après l'autre
Dont nous avons parlé tantôt,
Et fut si tant oun bon apôtre
Que j'en veux dire oun petit mot.
Qu'il nous suffise de comprendre
Qu'oun beau jour, je ne sais trop quand,
Du roi de France il devint gendre
...On s'imagine bien comment,
Et que—la ciel le garde et sauve!—
La beau-père de notre roi
Il s'appelait Charles-le-Chauve
...On peut bien deviner pourquoi.
Reprenant la fil de l'histoire,
Plus tard Ethelwolf s'en alla
Faire oun voyaige méritoire

A Rome, et fut si long par-là
Que, dans la cours de son absence,
Ethelwald, son fils, vrai coquin,
Avec le plus grande indécence
Prit le couronne et le fit sien.
Cet garçon, après deux années,
Finit son règne, par bonheur,
Et l'oun de ses frères puinées,
Ethelbert, fut sa successeur.
De cet-lui je dis peu de chose,
Attendu que je n'en sais rien.
D'Ethelred encore je n'ose
Risquer oun mot en mal ou bien,
Si ce n'est qu'il était la frère
De la monarque précédent
Et que, dit-on, il fut le père
Du roi fameuse Alfred-le-Grand.

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