Full-text resources of PSJD and other databases are now available in the new Library of Science.
Visit https://bibliotekanauki.pl

Refine search results

Journals help

  1. 34 Archivum Immunologiae et Therapiae Experimentalis

  2. 3 Postępy Higieny i Medycyny Doświadczalnej

  3. 1 Biotechnologia

  4. 1 Folia Biologica

Years help

  1. 1 2011

  2. 2 2008

  3. 2 2007

  4. 3 2006

  5. 7 2005

More...
Authors help

  1. 2 Biedron R.

  2. 2 Bobek M.

  3. 2 Brune B.

  4. 2 DeLeo F. R.

  5. 2 Kruzel M. L.

More...
Preferences help
Polish version English version Language
enabled [disable] Abstract
Number of results

Results found: 39

Number of results on page
first rewind previous Page / 2 next fast forward last

Search results

Search:
in the keywords:  INFLAMMATION
help Sort By:

help Limit search:
first rewind previous Page / 2 next fast forward last
1

Role of lactoferrin in development of inflammation

100%
Kruzel M. L.
|
EN
During acute inflammation, immune homeostasis is lost leading to destructive immunopathology. Homeostasis is normally dependent upon coordinated interactions among the various lymphoid, phagocytic and somatic cells that comprise the immune system. In general, these interactions are tightly regulated to obtain a balance between mechanisms necessary to eliminate harmful pathogens, and overaggressive responses leading to destruction of host tissue. Activation of immunoeffector cells results in pro-inflammatory cytokine up-regulation which in turn also activates the vascular endothelium. Through complex signaling, a positive feedback circuit is established which amplifies and sustains the activity of the inflammatory response resulting in the release of other cytokines and related molecules. If these responses are activated in an uncontrolled fashion with dissemination via the circulation, over the period of time, organs distant from the initial insult can be affected to produce multiple organ failure. Lactoferrin, an iron-binding glycoprotein, is considered an important mediator in host defense against the environmental insults in mammals. By virtue of iron sequestration lactoferrin can control the development of many oxidative stress-driven responses. The purpose of this review is to provide a comprehensive summary of research regarding lactoferrin and its role in homeostasis.
2

Lactoferrin and immunologic dissonance: clinical implications

80%
Kruzel M. L., Zimecki M.
Archivum Immunologiae et Therapiae Experimentalis
|
2002
|
vol. 50
|
issue 6
397-408
EN
Homeostasis is the maintenance of equilibrium in a biological system by means of positive and negative feedback control mechanisms that counteract influences tending toward physiological dissonance. At the molecular level, homeostasis is controlled by the network of the neuro-endocrine-immune system, in which lactoferrin plays a central role. The purpose of this review is to provide a comprehensive summary of a collaborative study established between the Hirszfeld Institute of Immunology and Experimental Therapy (Wroclaw, Poland) and the University of Texas Health Science Center (Huston, USA) regarding lactoferrin and its role in homeostasis. In our studies we focused on the immunoregulatory functions of lactoferrin, both in vitro and in vivo. We investigated the immune status of individuals subjected to different insults, including experimental endotoxemia in mice and surgery in humans. We also studied a lactoferrin-dependent delayed type hypersensitivity (DTH) response to evaluate some of the mechanisms by which lactoferrin can effectively substitute an adjuvant in vaccine.
3

Neutrophil recognition of bacterial DNA and Toll-like receptor 9-dependent and independent regulation of neutrophil function

80%
El_ K. D., Jozsef L., Filep J. G.
Archivum Immunologiae et Therapiae Experimentalis
|
2008
|
vol. 56
|
issue 1
41-53
EN
Neutrophils are essential for host defense and detect the presence of invading microorganisms through recognition of pathogen-associated molecular patterns. Among these receptors are Toll-like receptors (TLRs). Neutrophils express all known TLRs except for TLR3. TLR9, localized intracellularly, is to date the best characterized sensor for bacterial DNA, containing short sequences of unmethylated CpG motifs, though TLR9-independent intracellular DNA recognition mechanism(s) may also exist. Bacterial DNA has profound impact on neutrophil functions; it promotes neutrophil trafficking in vivo, induces chemokine expression, regulates expression of adhesion molecules, enhances phagocyte activity, and rescues neutrophils from constitutive apoptosis. TLR9 stimulation results in alterations in cellular redox balance, peroxynitrite formation, activation of the mitogen-activated protein kinase, PI3-kinase, and Jun N-terminal kinase pathways and/or nuclear factor ?B and AP-1. These features identify an important role for bacterial DNA and TLR9 signaling in the regulation of neutrophil functions that are critical for optimal expression as well as for resolution of the inflammatory response.
4

Mast cells and inflammation

80%
Stassen M., Hultner L., Muller C., Schmitt E.
Archivum Immunologiae et Therapiae Experimentalis
|
2002
|
vol. 50
|
issue 3
179-186
EN
Mast cells have long since been recognized as potent producers of a large panel of biological highly active mediators such as biogenic amines, arachidonic acid metabolites, cytokines and chemokines, but most of their biological functions had been elusive and speculative. By taking advantage of mast cell-deficient mice, the role of mast cells in a variety of experimental settings can now be studied in detail and such approaches have dramatically altered and enlarged our knowledge about mast cell biology and function. Herein we will focus on the role of mast cells in inflammatory reactions of diverse origin such as delayed type hypersensitivity, atopy, immune complex-mediated inflammation and innate immune responses. From a current point of view, there is no doubt that the most outstanding and beneficial feature of mast cells is their recently uncovered ability to rapidly induce a life-saving inflammatory response upon encountering microbes and microbial constituents. Nevertheless, the picture is also emerging that mast cells are deeply involved in the induction and maintenance of a variety of severe allergic and autoimmune diseases. However, a deeper understanding of their activation and immune-modulatory capacity might open a new window for the development of curative strategies.
5

Prostaglandins and inflammation: The cyclooxygenase controversy

80%
Morteau O.
Archivum Immunologiae et Therapiae Experimentalis
|
2000
|
vol. 48
|
issue 5
473-480
EN
Prostaglandins (PGs) are arachidonic acid metabolites produced by the action of the enzyme cyclooxygenase (COX). Although PGs are important mediators of inflammation in various diseases, they also are key factors in the physiological regulation of gastrointestinal and renal homeostasis. The finding that two distinct COX isoforms are responsible for PG synthesis has provided basis to the opposite actions of PGs in inflammation and homeostasis regulation. COX-1-derived PGs are thought to mediate cytoprotective actions on the gastrointestinal mucosa, whereas COX-2-derived PGs are assumed to display pro-inflammatory properties. This dichotomy has led to the development of selective inhibitors of COX-2 activity which are safer for the gastrointestinal mucosa than the classic inhibitors of both COX isoforms. However, some COX-2 antiinflammatory properties have been recently demonstrated in several experimental models of inflammation. These studies have raised some concern about the potential adverse effects of COX-2 selective inhibitors. In addition, there is evidence that COX-1 displays pro-inflammatory properties, depending on the organ and on the stage of the inflammatory response. This review will focus on the roles of COX-1 and COX-2 in inflammation, based on studies involving pharmacologic COX inhibitors as well as COX knockout mice, with a particular emphasis on the gastrointestinal tract
6

Leukotrienes ? mediators of inflammation

80%
Woszczek G., Pawliczak R., Kowalski M. L.
Postępy Higieny i Medycyny Doświadczalnej
|
2003
|
vol. 57
|
issue 5
593-610
EN
Leukotrienes are biologically active metabolites derived from arachidonic acid playing an important role in inflammatory responses. There are two main groups of leukotrienes: dihydroxy-leukotrienes (LTB4) and cysteinyl-leukotrienes (LTC4, LTD4, LTE4). By activating specific G-protein coupled receptors, leukotrienes take part in immune responses, like activation and chemotaxis of leukocytes. Several studies have shown that leukotrienes may play a significant role in pathomechanisms of inflammatory diseases of human airways, skin, digestive tract and heart.
7

Targeting the chemokine network in renal inflammation

80%
Eis V., Vielhauer V., Anders H.-J.
Archivum Immunologiae et Therapiae Experimentalis
|
2004
|
vol. 52
|
issue 3
164-172
EN
Chemokines and their receptors are involved in the pathogenesis of renal diseases. They mediate leukocyte recruitment and activation during initiation as well as progression of renal inflammation. Infiltrating leukocyte subpopulations contribute to renal damage by releasing inflammatory and profibrotic cytokines. All intrinsic renal cells are capable of chemokine secretion on stimulation in vitro. Expression of inflammatory chemokines correlates with renal damage and local accumulation of chemokine receptor-bearing leukocytes in a variety of animal models of renal diseases as well as in human biopsy studies. Chemokines and their respective receptors could represent new targets for therapeutic intervention in renal inflammatory disease states that often tend to progress to end-stage renal disease. This article summarizes the present data on the role of chemokines and their receptors in renal inflammation with special emphasis on our efforts to identify the chemokine receptors CCR1 and CCR2 as promising targets for therapeutic intervention.
8

Different pro-inflammatory and immunogenic potentials of Propionibacterium acnes and Staphylococcus epidermidis: implications for chronic inflammatory acne

80%
Bialecka A., Mak M., Biedron R., Bobek M., Kasprowicz A., Marcinkiewicz J.
Archivum Immunologiae et Therapiae Experimentalis
|
2005
|
vol. 53
|
issue 1
79-85
EN
Propionibacterium acnes (PA) and Staphyloccocus epidermidis (SE) are two major bacterial strains isolated from acne lesions. Nevertheless, only PA seems to be implicated in the pathogenesis of inflammatory acne vulgaris. Evidence for this, however, remains indirect and the precise role of PA in inflammatory acne is still a matter for conjecture. The aim of this study was to compare some pro-inflammatory and adjuvant properties of PA and SE. To determine some of the pathogenic, immunostimulatory, and pro-inflammatory properand ties of PA and SE, two experimental models of inflammation were used. In vivo; chronic inflammation was induced by intradermal injection of living bacteria into the ear. In vitro; peritoneal macrophages elicited by the bacteria were examined for their ability to generate reactive oxygen species (ROS), nitric oxide (NO), and cytokines. PA, but not SE, evoked mild local inflammation of infected ears. Macrophages elicited with PA produced more tumor necrosis factor ? and interleukin IL-12 than those induced with SE, while SE was a stronger inducer of IL-10 production. Both bacteria equally induced the generation of NO and ROS. In contrast, only PA showed adjuvant properties. The results of these studies indicate that SE, in contrast to PA, does not exert pro-inflammatory properties. Thus it is unlikely that SE may be implicated in the pathogenesis of inflammatory acne vulgaris.
9

The biology and pathology of hypoxia-ischemia: an update

80%
Clarkson A. N., Sutherland B. A., Appleton I.
Archivum Immunologiae et Therapiae Experimentalis
|
2005
|
vol. 53
|
issue 3
213-225
EN
After an hypoxic-ischemic (HI) insult, a multi-faceted complex cascade of events occurs that ultimately causes cell death and neurological damage to the central nervous system. The various cascades include, amongst others: immunological changes, such as the activation of the complement system and the generation of antibodies; increased inflammation through the actions of pro-inflammatory cytokines and chemokines; the production of reactive oxygen species leading to oxidative stress; and diminished mitochondrial function leading to the activation of apoptotic pathways and subsequent alteration in the function of neurons within the contralateral hemisphere. This review addresses the immunological aspects following HI, the role of various cytokines (both pro-inflammatory and anti-inflammatory) and chemokines after the induction of HI. In addition, the role of free radicals in producing HI-induced neurodegeneration and the contribution that mitochondrial dysfunction has in neuronal apoptotic cell death will be discussed. This review also covers the changes that the previously assumed 'internal control', the contralateral hemisphere, undergoes due to HI and describes the difficulties associated with therapy intended to prevent neuronal injury associated with HI.
10

The role of PTEN in allergic inflammation

80%
Lee Y. C.
|
EN
Bronchial asthma is a chronic inflammatory disease of the airways, characterized by airway eosinophilia, goblet cell hyperplasia with mucus hyper-secretion, and hyper-responsiveness to inhaled allergens and to non-specific stimuli. Eosinophil accumulation and subsequent activation in bronchial tissues play critical roles in the pathophysiology of bronchial asthma. Many inflammatory mediators attract and activate eosinophils via signal transduction pathways involving an enzyme phosphatidylinositol 3-kinase (PI3- kinase). Studies using wortmannin, a specific inhibitor of PI3-kinase, have revealed the involvement of PI3-kinase in the biochemical transduction of activation signals generated by many inflammatory mediators in eosinophils. Wortmannin prevents the development of airway inflammation, either by inhibiting the eosinophil infiltration of bronchial tissues or their activation on arrival. Phosphatase and tensin homologue deleted on chromosome 10 (PTEN) is part of a complex signaling system that affects a variety of important cell functions. PTEN opposes the action of PI3-kinase by dephosphorylating the signaling lipid phosphatidylinositol 3,4,5-triphosphate. Recently we have demonstrated that PTEN expression is diminished in airway epithelial cells of antigen-sensitized and -challenged mice. Administration of PI3-kinase inhibitors or adenoviruses carrying PTEN complementary DNA remarkably reduces eosinophil levels and inflammation. One likely mechanism for this reduction is PTEN-mediated eosinophil degranulation and suppression of interleukin (IL)-4 and IL-5. These findings indicate that use of PTEN may be a good therapeutic strategy for the management of allergic inflammation.
11

Do changes in iron metabolism contribute to the acceleration of the atherosclerosis process?

80%
Formanowicz D.
Biotechnologia
|
2011
|
issue 2
180-192
EN
There are several risk factors whose association with atherosclerosis, a chronic disease with complicated etiology, is well established, including age, gender, smoking, lipids metabolism disorders, diabetes mellitus, obesity and reduced physical activity. Surprisingly, many cardiovascular related deaths occur in individuals without standard risk factors, so it has been suggested that these cases must be the result of other factors, previously not taken into account. This phenomenon resulted in the development of research focused on finding new risk factors. In 1981, Sullivan first postulated the so-called 'iron hypothesis', suggesting that the regular menstrual iron loss, rather than other known effects of estrogen, protects women against coronary heart disease. It is widely believed at present, that iron is an essential catalyst in the oxidation and oxidative modification of low-density lipoprotein cholesterol which appears to be one of the pivotal steps in the early phase of the formation of the atherosclerotic plaque. Thus, iron depletion through menstrual loss might reduce oxidative stress and beneficially affect atherogenesis. Stored iron appears to be essential in the process of atherogenesis which is strictly required for normal cellular metabolism but also serves as a reservoir from which toxic-active iron can be liberated under atherogenic stimuli and result in lipid peroxidation. In this process, two pathways i.e., iron homeostasis metabolic pathway and metabolic pathways involving proinflammatory cytokines are closely interconnected. In human monocytes, these cytokines also increase the uptake of non-transferrin-bound iron, via the stimulation of divalent metal transporter- 1 synthesis and cause iron retention by down-regulating ferroportin synthesis. It has been found recently that iron depositions are prominent in human atherosclerosis lesions. It can therefore be concluded that the results of scientific research, particularly those of the last ten years, provide a strong pathological basis to support the role of iron metabolism alterations in vascular damage and in the progression of atherosclerosis process.
12

Immunomodulatory effects of HMG-CoA reductase inhibitors

80%
Danesh F. R., Anel R. L., Zeng L., Lomasney L., Sahai A., Kanwar Y. S.
|
EN
3-Hydroxy-3-methyl-glutaryl coenzyme A (HMG-CoA) reductase inhibitors or statins are competitive inhibitors of the rate limiting enzyme in cholesterol synthesis. Several clinical trials have shown a marked reduction in cholesterol levels associated with decreased cardiovascular mortality in patients treated with statins. However, more recent observations have suggested that the clinical benefits of statins may be, at least in part, independent of the effect of statins on cholesterol synthesis. These so-called pleiotropic or cholesterol-independent effects of statins could be the result of reduction in the formation of intermediaries in the mevalonate pathway as statins by inhibiting L-mevalonic acid synthesis also prevent the production of isoprenoids in the cholesterol biosynthetic pathway. Isoprenoids serve as important lipid attachments for the posttranslational modification of a variety of proteins such as small GTP-binding proteins of the Ras superfamily implicated in intracellular signaling. The list of different pleitropic effects of statins is still growing and include among others direct effects of statins on modulating endothelial function, decreasing oxidative stress, and more recently anti-inflammatory and immunomodulatory actions of statins. For instance, statins decrease T cell activation, the recruitment of inflammatory cells into atherosclerotic lesions, and inhibit IFN-gamma expression of MHCII on antigen-presenting cells. This review article summarizes the anti-inflammatory and immunomodulatory effects of statins and thus provides a new rationale to use statins as a new class of immunosuppressive agents.
13

Using knockout mice to study experimental meningitis

80%
Paul R., Koedel U., Pfister H.-W.
Archivum Immunologiae et Therapiae Experimentalis
|
2003
|
vol. 51
|
issue 5
315-326
EN
Despite the use of antibiotics, the prognosis of bacterial meningitis is still poor due to central nervous system (CNS) complications, such as brain edema formation, cerebrovascular alterations, and intracranial hemorrhage. Experimental studies with animal models have given new insights into its pathophysiology during the acute phase of the disease. In recent years, genetically engineered mice have become a powerful tool in investigating the role of particular genes by targeted deletion and have also been applied in bacterial meningitis research. By using knockout mice, new knowledge of the roles of the different cytokines, proteases, and oxidants involved in the inflammatory cascade has emerged. In the future, temporal and cell type-specific control of gene expression will provide even more information on the impact of a particular gene on meningitis-induced brain damage.
14

Peroxisome proliferator-activated receptor gamma (PPARgamma) and sepsis

80%
von_ K. A., Soller M., Brune B.
Archivum Immunologiae et Therapiae Experimentalis
|
2007
|
vol. 55
|
issue 1
19-25
EN
This review describes the role of the nuclear hormone receptor PPARgamma as a double-edged sword in sepsis. On the one hand, PPARgamma inhibits pro-inflammatory gene expression, predominantly by scavenging transcription factors and their cofactors, thus preventing them from binding to their cognate binding sites in the promoters of target genes. The expressions of the affected genes, such as those for inducible nitric oxide synthase, TNF-alpha, or IL-1beta are repressed. Therefore, PPARgamma is suggested to be beneficial in hyper-inflammatory diseases, such as sepsis. In n animal models of sepsis, PPARgamma agonist pretreatment auspiciously attenuated inflammation compared with control animals, accompanied by their improved survival rate. On the other hand, PPARgamma provokes apoptosis, which in the hyper-inflammatory phase of sepsis might be helpful because the number of immune cells, such as monocytes, macrophages, and neutrophils, involved in secreting high amounts of pro-inflammatory mediators will be reduced. In contrast, during the anti-inflammatory phase, cell death of immune cells, especially of T lymphocytes, is supposed to be deleterious. Under these circumstances, a second infection cannot be adequately answered, thus causing septic shock and multi-organ dysfunction syndrome. Therefore the role of PPARgamma is still ambiguous. Particularly its role in initiating apoptosis awaits further clarification to finally elucidate its impact on sepsis development.
15

CSF-1 as a regulator of macrophage activation and immune responses

80%
Sweet M. J., Hume D. A.
Archivum Immunologiae et Therapiae Experimentalis
|
2003
|
vol. 51
|
issue 3
169-177
EN
Macrophage activation is a key determinant of susceptibility and pathology in a variety of inflammatory diseases. The extent of macrophage activation is tightly regulated by a number of pro-inflammatory cytokines (e.g. IFN-gamma, IL-2, GM-CSF, IL-3) and anti-inflammatory cytokines (e.g. IL-4, IL-10, TGF-beta). Macrophage colony stimulating factor (CSF-1/M-CSF) is a key differentiation, growth and survival factor for monocytes/macrophages and osteoclasts. The role of this factor in regulating macrophage activation is often overlooked. This review will summarise our current understanding of the effects of CSF-1 on the activation state of mature macrophages and its role in regulating immune responses.
16

New target against inflammatory diseases: transglutaminase 2

80%
Kim S.-Y.
Archivum Immunologiae et Therapiae Experimentalis
|
2004
|
vol. 52
|
issue 5
332-337
EN
Transglutaminase (TGase) 2 is an enzyme that is widely used in many biological systems for generic tissue stabilization or immediate defense for wounds. Many reports showed that TGase 2 is aberrantly activated in tissues and cells and contributes to a variety of diseases, including neurodegenerative diseases and autoimmune diseases. In most cases, TGase 2 appears to be a factor in the formation of inappropriate proteinaceous aggregates that may be cytotoxic. However, in other cases, such as celiac disease, arthritis, lupus, and amyotrophic lateral sclerosis, TGase 2 is involved in the generation of autoantibodies. This suggests the possibility that inappropriate expression and/or presentation of TGase 2 to T cells might contribute to these diseases in genetically predisposed individuals. We and others have found that TGase 2 expression is also increased in the inflammation process. Furthermore, we also demonstrated a reversal of inflammation by TGase inhibition. This review will examine a possibility of TGase inhibitors as therapeutic agents in a variety of inflammatory diseases.
17

Apoptosis in human polymorphonuclear leukocytes: Searching for a genetic roadmap

80%
Kobayashi S. D., DeLeo F. R.
Archivum Immunologiae et Therapiae Experimentalis
|
2003
|
vol. 51
|
issue 1
1-8
EN
Polymorphonuclear leukocytes (PMNs or neutrophils) are essential components of the innate immune system in humans and function primarily to eliminate invading microorganisms. Neutrophil influx to sites of infection is desirable because it also initiates an inflammatory response. Paradoxically, PMNs are also intimately associated with inflammatory disease. As part of normal neutrophil turnover in humans and to limit inflammatory potential, PMNs undergo programmed cell death or apoptosis. Several host factors, including cytokines and growth factors, are capable of extending neutrophil survival, and thus capacity to fight infection. On the other hand, phagocytosis of bacterial pathogens generally accelerates PMN apoptosis. Due in part to the extensive complexity of programmed cell death, relatively little is known about signaling pathways that govern these processes in PMNs. Recently, microarray strategies have been employed to gain an understanding of these processes in activated PMNs, and new evidence indicates that gene transcription is important in the regulation of neutrophil apoptosis and thus inflammation. A series of provocative discoveries led to the hypothesis that neutrophil programmed cell death is the result of an apoptosis differentiation program, a final stage of transcriptionally regulated PMN maturation or hematopoietic differentiation. Further characterization of the apoptosis differentiation program and associated biochemical pathways in mature PMNs will likely yield important insights into the resolution of inflammation and infection.
18

Inflammation in periodontal tissues in response to mechanical forces

80%
Yamaguchi M., Kasai K.
Archivum Immunologiae et Therapiae Experimentalis
|
2005
|
vol. 53
|
issue 5
388-398
EN
Orthodontic forces are known to produce mechanical damage and inflammatory reactions in the periodontium and dental pulp, as well as inflammatory mediators, e.g. prostaglandins, interleukin (IL)-1, IL-6, tumor necrosis factor a, and receptor activator of nuclear factor kB ligand, in the periodontal ligament (PDL) and dental pulp. We have studied the effects of aging on the production of inflammatory mediators in the PDL using in vitro and in vivo methods and found that aging of PDL tissues may be an important factor in the severity of periodontal disease through a higher production of inflammatory mediators in response to mechanical forces. Further, the levels of inflammatory mediators in gingival crevicular fluid, an osmotically mediated inflammatory exudate found in the gingival sulcus, have been shown to be significantly elevated during orthodontic treatment. In order to reduce inflammation, low-level laser therapy has been recently studied in vivo and in vitro by many investigators as a substitute for anti-inflammatory drugs. Clinical and experimental studies have shown that low-level laser irradiation reduces orthodontic post-adjustment inflammation. We believe that orthodontic forces (mechanical forces) may play an important role in periodontal inflammation and that low-level laser therapy may be useful for its inhibition.
19

PPAR ? an important regulator of monocyte/macrophage function

80%
von K. A., Brune B.
Archivum Immunologiae et Therapiae Experimentalis
|
2003
|
vol. 51
|
issue 4
219-226
EN
Regulation of monocyte/macrophage function is important to coordinate immune responses. Their contact with invading pathogens activates signaling pathways that provoke pro-inflammatory gene expression and thus causing a locally restricted inflammation. Recently, the peroxisome proliferator activated receptor (PPAR) has been identified to antagonize pro-inflammatory responses in monocytes/macrophages causing an anti-inflammatory and/or desensitized phenotype to predominate. For PPAR general mechanisms in facilitating the transition from a pro- to an anti-inflammatory phenotype have been elucidated. PPAR is a member of the nuclear receptor superfamily and activated upon endogenous as well as exogenous agonist binding. Here we focus on its role in monocyte/macrophage biology in affecting inflammation. Summarizing current information, a model is proposed, giving rise to potential new therapeutic possibilities for the treatment of diseases presumably involving PPAR-dependent regulatory circuits.
20

Modulation of the immune response by extracellular matrix proteins

80%
Morwood S. R., Nicholson L. B.
Archivum Immunologiae et Therapiae Experimentalis
|
2006
|
vol. 54
|
issue 6
367-374
EN
Inflammation entrains a focused and coordinated response from many different elements. Soluble factors such as chemokines and cytokines direct the recruitment, differentiation, and fate of leukocytes. Cells and pathogens are killed and consumed, yet where the response is effective, inflammation will melt away, leaving a healthy functioning tissue. All this commonly takes place in an environment known as the extracellular matrix (ECM). The ECM is not a passive partner in the process and recent work demonstrates the important role that proteins found in this environment play in connecting different parts of the immune response together. In this review we will focus on these connections and the proteins that make them. One emerging trend that we will highlight is the ability of endogenous molecules to interact with receptors that are better known as sensors of the molecular fingerprints of infection. We propose that this may be particularly relevant in the context of autoimmunity, since the provision of such signals may be crucial in breaking tolerance.
first rewind previous Page / 2 next fast forward last
JavaScript is turned off in your web browser. Turn it on to take full advantage of this site, then refresh the page.