Qui est en ligne ?
Il y a en tout 29 utilisateurs en ligne :: 0 Enregistré, 0 Invisible et 29 Invités Aucun
Le record du nombre d'utilisateurs en ligne est de 480 le Jeu 16 Sep - 4:29
Derniers sujets
Les mastocytes et leurs fonctions biologiques,
4 participants
DOC DZ...La Communauté des Etudiants et Praticiens en Médecine :: LES MEDECINS ... :: CLINIQUE ET INTERNAT
:: 3eme :: immunologie
Page 1 sur 1
Les mastocytes et leurs fonctions biologiques,
Le nouveau concept des mastocytes et leurs fonctions (physiologique et pathologique) profitez mes amis, c'est un cours du jamais vu!!!!!!!!!!
Mast cell proteases and host defense
Mast cells are strategically located very near sites where the body comes in contact with the external environment, which is a prime location for the initiation and modulation of innate immune responses. Indeed, mast cells can provide important contributions to innate bacterial clearance, at least in part by enhancing the recruitment of neutrophils to the site of infection. Many in vitro or in vivo studies have provided additional evidence that mast cells can enhance host defense through direct effects on pathogens by initiating and modulating the inflammation associated with innate immune responses and perhaps by initiating adaptive immune responses to pathogens.
Another protective function of mast cells during innate responses to bacterial infection is to limit the toxicity of certain products generated by the host, which can have adverse effects at high concentrations. For example, mast cells can limit the toxicity of the peptide endothelin 1 (ET-1), whose concentrations are much higher during acute bacterial peritonitis and sepsis, by releasing proteases stored in their granules that can degrade this peptide. ET-1 has high homology to sarafotoxins (the most toxic components of venom from the Israeli mole viper (Atractaspis engaddensis)). Mast cells can substantially enhance resistance to the pathology and mortality induced in mice by the venoms from A. engaddensis and two other poisonous snakes and that of the honeybee66. Both short hairpin RNA and pharmacological methods have been used to show that a mast cell–mediated decrease in endogenous (ET-1) and exogenous (sarafotoxin) toxic peptides is dependent on the activity of carboxypeptidase A3 (CPA3); however, mast cells that lack CPA3 concomitantly lack mast cell protease 5 (MCP-5). In an elegant study, a mutant mouse has been generated bearing two amino acid substitutions that render CPA3 catalytically inactive without affecting the expression of other proteases. Using this mutant, the authors confirm that mast cell–mediated innate defense against ET-1 and sarafotoxin is dependent on CPA3 activity, and they define the molecular mechanism by which CPA3 inactivates these toxins.
Mast cell proteases also can contribute to resistance to infection with parasites. For example, delayed expulsion of the adult helminth and increased deposition of larvae in muscles occur in MCP-1-deficient mice infected with Trichinella spiralis. MCP-6 is important for the clearance of chronic T. spiralis infection; the recruitment of eosinophils to T. spiralis larvae and the elimination of larvae in chronically infected skeletal muscle are lower in MCP-6-deficient mice. Because eosinophil infiltration around T. spiralis larvae is also lower in IgE-deficient mice, the authors suggest that mast cells and, more specifically, MCP-6 link adaptive and innate immunity in the chronic phase of T. spiralis infection.
Mast cells in cardiovascular disorders
Several lines of evidence have linked mast cells to the development of a variety of chronic inflammatory disorders, including cardiovascular disease. Because mast cells are found in the heart and, in humans, around coronary arteries and in atherosclerotic lesions, several groups have proposed that mast cells may contribute to the pathogenesis of atherogenesis. Indeed, targeted activation of perivascular mast cells promotes atherogenesis and plaque destabilization in apolipoprotein E–deficient mice. By crossing atherosclerosis-prone mice deficient in low-density lipoprotein receptor with C57BL/6-KitW-sh/W-sh mice, others have provided in vivo evidence that mast cells can contribute to atherosclerosis, as smaller lesions with fewer inflammatory cell (macrophage and T cell) infiltrates are noted in the absence of mast cells. There is evidence that mast cells promote atherosclerosis in this setting by releasing proinflammatory cytokines (IL-6 and interferon-) that augment the expression of matrix-degrading proteases99. This group has also reported that mast cells contribute to the pathogenesis of elastase-induced abdominal aortic aneurysms in mice, as C57BL/6-KitW-sh/W-sh mice fail to develop such aneurysms. They show that the formation of such aneurysms in this model requires mast cell–derived IL-6 and IFN-, but not TNF, and that mast cells increase the expression of matrix-degrading proteases, the apoptosis of smooth muscle cells and microvessel growth. Similarly, others have shown that the formation of such aneurysms after periaortic application of calcium chloride (accompanied by more mast cells and T cells, activation of matrix metalloproteinase 9, and angiogenesis in the aortic tissue) is impaired in mast cell–deficient Ws/Ws rats.
Mast cells in cancer
The importance of a possible functional link between chronic inflammation and cancer has long been recognized; for example, treatment with nonsteroidal anti-inflammatory drugs, which can inhibit chronic inflammation, decreases the risk of several cancers. Most tumors contain inflammatory cells, including mast cells, which have potential effects that might either benefit the tumor or contribute to tumor resistance or rejection. Experiments with WBB6F1-KitW/W-v mice have provided evidence that mast cells can facilitate angiogenesis during early stages of skin carcinogenesis. Pharmacological approaches (cromolyn) and genetic approaches (C57BL/6-KitW-sh/W-sh mice) suggest that mast cells also may be required for the angiogenesis and macroscopic expansion of c-Myc-induced pancreatic -cell tumors. Although cromolyn is widely characterized as a 'mast cell stabilizer' (as an agent that blocks the release of mast cell mediators after appropriate activation of the cell) that suppresses mouse mast cell function in vivo, its molecular targets are neither fully defined nor restricted to mast cells. Moreover, because c-Kit signaling has been shown to be important for angiogenesis and cell lineages other than mast cells are affected by the Kit mutation in C57BL/6-KitW-sh/W-sh mice, it will be useful to assess whether engraftment of the C57BL/6-KitW-sh/W-sh mice with mast cells can restore wild-type responsiveness in this model of tumor progression. However, these results and others collectively indicate that certain tumors may 'hijack' certain functions of mast cells to facilitate angiogenesis and contribute to tumor survival.
Although other evidence also suggests that mast cells can promote tumorigenesis and tumor progression, there are some tumor models in which mast cells seem to have functions that favor the host. For example, one report has demonstrated a protective a function for mast cells in colorectal tumorigenesis. Mice resulting from the crossing of C57BL/6-KitW-sh/W-sh mice with mice that have multiple intestinal neoplasia (a model for early intestinal tumorigenesis) have a greater frequency and size of adenomas, whereas they have less tumor cell apoptosis and eosinophil infiltration. The authors of that study suggest that the net contributions of mast cells in various tumor models may favor the host or the tumor depending on the specific tumor model, genetic variables (both germline and tumor specific) and microenvironmental factors (such as intestinal flora in gastrointestinal tumors). The story is probably as complicated (if not more so) in humans, given that humans, as well as their colonic neoplasms, are so diverse.
À bientôt, excusez si mon texte est un peu long,
@
En fin
New evidence indicating that mast cells can contribute to the pathology of cardiovascular diseases and certain cancers (at least in rodents) continues to tarnish the reputation of this enigmatic cell. However, this 'bad guy' image is increasingly being challenged and, to some extent, overshadowed by identification of the many protective functions mast cells can serve in both innate and adaptive immune responses and even in host responses to some tumors. But many issues of mast cell biology remain to be resolved. For example, certain features of mouse mast cell phenotype and/or function can vary considerably among different strains of mice.[img][/img]
Mast cell proteases and host defense
Mast cells are strategically located very near sites where the body comes in contact with the external environment, which is a prime location for the initiation and modulation of innate immune responses. Indeed, mast cells can provide important contributions to innate bacterial clearance, at least in part by enhancing the recruitment of neutrophils to the site of infection. Many in vitro or in vivo studies have provided additional evidence that mast cells can enhance host defense through direct effects on pathogens by initiating and modulating the inflammation associated with innate immune responses and perhaps by initiating adaptive immune responses to pathogens.
Another protective function of mast cells during innate responses to bacterial infection is to limit the toxicity of certain products generated by the host, which can have adverse effects at high concentrations. For example, mast cells can limit the toxicity of the peptide endothelin 1 (ET-1), whose concentrations are much higher during acute bacterial peritonitis and sepsis, by releasing proteases stored in their granules that can degrade this peptide. ET-1 has high homology to sarafotoxins (the most toxic components of venom from the Israeli mole viper (Atractaspis engaddensis)). Mast cells can substantially enhance resistance to the pathology and mortality induced in mice by the venoms from A. engaddensis and two other poisonous snakes and that of the honeybee66. Both short hairpin RNA and pharmacological methods have been used to show that a mast cell–mediated decrease in endogenous (ET-1) and exogenous (sarafotoxin) toxic peptides is dependent on the activity of carboxypeptidase A3 (CPA3); however, mast cells that lack CPA3 concomitantly lack mast cell protease 5 (MCP-5). In an elegant study, a mutant mouse has been generated bearing two amino acid substitutions that render CPA3 catalytically inactive without affecting the expression of other proteases. Using this mutant, the authors confirm that mast cell–mediated innate defense against ET-1 and sarafotoxin is dependent on CPA3 activity, and they define the molecular mechanism by which CPA3 inactivates these toxins.
Mast cell proteases also can contribute to resistance to infection with parasites. For example, delayed expulsion of the adult helminth and increased deposition of larvae in muscles occur in MCP-1-deficient mice infected with Trichinella spiralis. MCP-6 is important for the clearance of chronic T. spiralis infection; the recruitment of eosinophils to T. spiralis larvae and the elimination of larvae in chronically infected skeletal muscle are lower in MCP-6-deficient mice. Because eosinophil infiltration around T. spiralis larvae is also lower in IgE-deficient mice, the authors suggest that mast cells and, more specifically, MCP-6 link adaptive and innate immunity in the chronic phase of T. spiralis infection.
Mast cells in cardiovascular disorders
Several lines of evidence have linked mast cells to the development of a variety of chronic inflammatory disorders, including cardiovascular disease. Because mast cells are found in the heart and, in humans, around coronary arteries and in atherosclerotic lesions, several groups have proposed that mast cells may contribute to the pathogenesis of atherogenesis. Indeed, targeted activation of perivascular mast cells promotes atherogenesis and plaque destabilization in apolipoprotein E–deficient mice. By crossing atherosclerosis-prone mice deficient in low-density lipoprotein receptor with C57BL/6-KitW-sh/W-sh mice, others have provided in vivo evidence that mast cells can contribute to atherosclerosis, as smaller lesions with fewer inflammatory cell (macrophage and T cell) infiltrates are noted in the absence of mast cells. There is evidence that mast cells promote atherosclerosis in this setting by releasing proinflammatory cytokines (IL-6 and interferon-) that augment the expression of matrix-degrading proteases99. This group has also reported that mast cells contribute to the pathogenesis of elastase-induced abdominal aortic aneurysms in mice, as C57BL/6-KitW-sh/W-sh mice fail to develop such aneurysms. They show that the formation of such aneurysms in this model requires mast cell–derived IL-6 and IFN-, but not TNF, and that mast cells increase the expression of matrix-degrading proteases, the apoptosis of smooth muscle cells and microvessel growth. Similarly, others have shown that the formation of such aneurysms after periaortic application of calcium chloride (accompanied by more mast cells and T cells, activation of matrix metalloproteinase 9, and angiogenesis in the aortic tissue) is impaired in mast cell–deficient Ws/Ws rats.
Mast cells in cancer
The importance of a possible functional link between chronic inflammation and cancer has long been recognized; for example, treatment with nonsteroidal anti-inflammatory drugs, which can inhibit chronic inflammation, decreases the risk of several cancers. Most tumors contain inflammatory cells, including mast cells, which have potential effects that might either benefit the tumor or contribute to tumor resistance or rejection. Experiments with WBB6F1-KitW/W-v mice have provided evidence that mast cells can facilitate angiogenesis during early stages of skin carcinogenesis. Pharmacological approaches (cromolyn) and genetic approaches (C57BL/6-KitW-sh/W-sh mice) suggest that mast cells also may be required for the angiogenesis and macroscopic expansion of c-Myc-induced pancreatic -cell tumors. Although cromolyn is widely characterized as a 'mast cell stabilizer' (as an agent that blocks the release of mast cell mediators after appropriate activation of the cell) that suppresses mouse mast cell function in vivo, its molecular targets are neither fully defined nor restricted to mast cells. Moreover, because c-Kit signaling has been shown to be important for angiogenesis and cell lineages other than mast cells are affected by the Kit mutation in C57BL/6-KitW-sh/W-sh mice, it will be useful to assess whether engraftment of the C57BL/6-KitW-sh/W-sh mice with mast cells can restore wild-type responsiveness in this model of tumor progression. However, these results and others collectively indicate that certain tumors may 'hijack' certain functions of mast cells to facilitate angiogenesis and contribute to tumor survival.
Although other evidence also suggests that mast cells can promote tumorigenesis and tumor progression, there are some tumor models in which mast cells seem to have functions that favor the host. For example, one report has demonstrated a protective a function for mast cells in colorectal tumorigenesis. Mice resulting from the crossing of C57BL/6-KitW-sh/W-sh mice with mice that have multiple intestinal neoplasia (a model for early intestinal tumorigenesis) have a greater frequency and size of adenomas, whereas they have less tumor cell apoptosis and eosinophil infiltration. The authors of that study suggest that the net contributions of mast cells in various tumor models may favor the host or the tumor depending on the specific tumor model, genetic variables (both germline and tumor specific) and microenvironmental factors (such as intestinal flora in gastrointestinal tumors). The story is probably as complicated (if not more so) in humans, given that humans, as well as their colonic neoplasms, are so diverse.
À bientôt, excusez si mon texte est un peu long,
@
En fin
New evidence indicating that mast cells can contribute to the pathology of cardiovascular diseases and certain cancers (at least in rodents) continues to tarnish the reputation of this enigmatic cell. However, this 'bad guy' image is increasingly being challenged and, to some extent, overshadowed by identification of the many protective functions mast cells can serve in both innate and adaptive immune responses and even in host responses to some tumors. But many issues of mast cell biology remain to be resolved. For example, certain features of mouse mast cell phenotype and/or function can vary considerably among different strains of mice.[img][/img]
Immunology- Membre Spécial
- Messages : 823
inscrit(e) le: : 02/05/2009
Re: Les mastocytes et leurs fonctions biologiques,
j'ai un beau schéma mais je ne peux le joindre
Immunology- Membre Spécial
- Messages : 823
inscrit(e) le: : 02/05/2009
Re: Les mastocytes et leurs fonctions biologiques,
tt ca pour une mastocyte de 8 à 20 µm de diamètre waw kel malignel
merci immuno pour c nouveautès
merci immuno pour c nouveautès
dr.bochra- Super Moderateur
- Messages : 1275
inscrit(e) le: : 27/04/2009
Localisation : .
Re: Les mastocytes et leurs fonctions biologiques,
j'ai mis presque une heure pour tenter d'en tirer profit ,je ne vais pas me décourager je vais y arriver inchallah merci !!!!
dr mirion- Membre Actif
- Messages : 2131
inscrit(e) le: : 27/04/2009
Localisation : entre A et B
la prisonniere d ses lois- Membre Actif
- Messages : 110
inscrit(e) le: : 23/07/2009
Localisation : SBA
Sujets similaires
» Drainage de la plèvre : les techniques et leurs pièges
» Cours de Biologie Moléculaire et Génétique
» Le guide des examens biologiques
» Analyses biologiques : sujets de B.T.S corrigés
» examens biologiques complementaires en cancerologie .
» Cours de Biologie Moléculaire et Génétique
» Le guide des examens biologiques
» Analyses biologiques : sujets de B.T.S corrigés
» examens biologiques complementaires en cancerologie .
DOC DZ...La Communauté des Etudiants et Praticiens en Médecine :: LES MEDECINS ... :: CLINIQUE ET INTERNAT
:: 3eme :: immunologie
Page 1 sur 1
Permission de ce forum:
Vous ne pouvez pas répondre aux sujets dans ce forum
|
|
Lun 25 Mar - 20:37 par faridw27
» Coloscopie virtuelle, imagerie médicale pratique
Ven 15 Mar - 22:32 par lesconnaissances
» TOUTE L'EMBRYOLOGIE DE LA FECONDATION JUSQU'A L'INFINI!!!
Mar 12 Mar - 8:53 par Ezéchiel
» Histologie fonctionnelle Manuel et Atlas de Wheater, Exclusivité Doc DZ
Lun 4 Mar - 15:55 par Guabos
» Dermatologie infectieuse
Dim 25 Fév - 11:56 par Alasko
» Gynécologie Obstétrique Fertilité & Sénologie , 2020
Mar 30 Jan - 20:21 par telechargers
» plus de 3300 question à réponses ouvertes courtes de sémiologie
Jeu 9 Nov - 10:13 par DSDIAMIL
» ARBRES DECISIONNELS EN PEDIATRIE
Mer 8 Nov - 18:34 par Ikramamro61
» Imagerie des Urgences 2019
Lun 6 Nov - 14:06 par Drdemb
» Guide du bon usage examens d'imagerie médicale
Lun 6 Nov - 14:01 par Drdemb
» Recommandations de bonne pratique et Perfectionnement en Pediatrie en Exclusivité pour Vous
Sam 4 Nov - 19:48 par Ikramamro61
» Besoin d’un livre
Jeu 26 Oct - 13:29 par Mumu
» précis d'obstétrique par robert merger
Mar 24 Oct - 2:43 par hlyes1973
» 18 cours de Pharmacologie Spéciale
Lun 11 Sep - 17:49 par hadjardz
» collection de cours orthopedie pour externes internes et residents
Lun 11 Sep - 14:00 par doc.richie73
» LIVRE"Pathologies vasculaires oculaires" rapport SFO 2008
Mar 13 Juin - 18:27 par vasileva722
» la collection Facile (ELSEVIER / MASSON)
Lun 1 Mai - 10:25 par lesconnaissances
» Collection Clinique et Semiologie:
Mar 4 Avr - 1:46 par ABDOUL-DJALIL
» Cahiers d'anatomie
Mar 4 Avr - 1:26 par ABDOUL-DJALIL
» Précis d'obstétrique
Mer 22 Mar - 20:03 par Douniakd
» Précis d'obstétrique
Mer 22 Mar - 20:02 par Douniakd
» Mémento de pathologie 5e édition 2017 Eclusivité Doc DZ
Jeu 10 Nov - 14:01 par Lamy
» appareil urinaire
Dim 2 Oct - 23:21 par landrykp123
» Merci de signaler les liens morts ici !
Mer 21 Sep - 12:27 par khaled-doc
» La biochimie en 1001 QCM PCEM
Mer 31 Aoû - 9:30 par bentolila
» Livre Echographie 4 eme édition " imagerie médicale formation "
Dim 14 Aoû - 23:26 par miz10
» Collection Cas cliniques en imagerie ...5 Livres pour vous
Dim 14 Aoû - 23:12 par miz10
» Les Infections Intra-Abdominales Aiguës
Mer 18 Mai - 14:40 par HINAULT
» 50 cas clinique pediatrie.
Mer 23 Mar - 5:48 par AmiraB0304
» guide des medicaments injectables/adulte
Ven 10 Déc - 23:57 par IDE Bamba
» Protocoles médicaux
Ven 10 Déc - 23:51 par IDE Bamba
» physio humaine
Mer 28 Juil - 17:57 par Sebastien KALOMBO
» Comment télécharger nos documents et fichiers
Mer 28 Juil - 17:32 par Sebastien KALOMBO
» MIKBOOK : les cahiers de l'internat 3eme edition
Mer 14 Juil - 12:55 par doctoresse18
» Guide de prise en charge de la diarhée chez l'enfant
Ven 25 Juin - 14:01 par waju
» logiciel vidal expert 2013 avec activation jusqu'à 2100
Jeu 20 Mai - 18:11 par salih
» La Collection Campus illustré et référence : 8 livres pour vous...
Jeu 18 Mar - 7:53 par Dontstop
» 20 livres de la Collection Médecine KB dont 3 conformes aux ECNi
Mar 16 Mar - 15:34 par Le Fondateur
» MAJBOOK - Le livre du Major editions Med-Line
Mar 16 Mar - 15:29 par Le Fondateur
» La Collection Ophtalmologie (Elsevier-Masson-Springer)
Lun 1 Fév - 10:16 par Le Fondateur