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. 15 Archivum Immunologiae et Therapiae Experimentalis

  2. 3 Acta Neurobiologiae Experimentalis

  3. 3 Journal of Applied Genetics

  4. 3 Postępy Higieny i Medycyny Doświadczalnej

  5. 2 Biotechnologia

More...
Years help

  1. 1 2010

  2. 3 2008

  3. 3 2007

  4. 1 2006

  5. 3 2005

More...
Authors help

  1. 2 Stokowska W.

  2. 1 AkaiwaM.

  3. 1 Anderson S. K.

  4. 1 Arima K.

  5. 1 Bagot M.

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

Results found: 28

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

Search results

Search:
in the keywords:  RECEPTOR
help Sort By:

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

Peroxisome proliferator-activated receptors (PPARs) in cardiovascular pathophysiology

100%
Beltowski J., Wojcicka G., Jamroz A.
Postępy Higieny i Medycyny Doświadczalnej
|
2003
|
vol. 57
|
issue 2
199-217
EN
Peroxisome proliferator-activated receptors (PPARs) are ligand-activated nuclear receptors which regulate the expression of target genes. Three types of PPAR have been identified: PPAR alpha, PPAR beta/delta and PPAR gamma. The known endogenous PPAR ligands are polyunsaturated fatty acids and eicosanoids, such as 15-deoxy-delta12,14-prostaglandin J2 and leukotriene B4. Two classes of drugs, fibrates and thiazolidinediones bind to PPAR alpha and PPAR gamma, respectively. PPARs are involved in the regulation of the lipid metabolism and adipogenesis but are also expressed in the vasculature. PPARs activators inhibit inflammatory reactions within the vascular wall, inhibit vascular smooth muscle cells migration and proliferation and affect foam cells formation by changing the expression different animal models of hypertension as well as in humans. PPAR gamma ligands inhibit the development of atherosclerosis in LDL receptor deficient and apolipoprotein E deficient mice and in diabetic humans. PPARgamma agonists have also been shown to attenuate myocardial hypertrophy and protect against ischemia-reperfusion injury.
2

Interleukin-12 (IL-12) and its receptor

100%
Szeliga J., Goscicka T.
Postępy Higieny i Medycyny Doświadczalnej
|
2002
|
vol. 56
|
issue 2
185-199
EN
This article reviews of recent data on the structure of IL-12 and the function of its receptor (IL-12R). It presents a new opinion on the role of its subunits in the cytokine activity and on the signal transmission via IL-12R in the process of cell activation by IL-12
3

Regulation of local immunity by airway epithelial cells

80%
Mayer A. K., Dalpke A. H.
|
2007
|
vol. 55
|
issue 6
353-363
EN
Epithelial cells are the first line of defense against invading microbial pathogens. They are important contributors to innate mucosal immunity and generate various and sophisticated anti-microbial defense mechanisms, including the formation of a tight barrier and secretion of anti-microbial substances as well as inflammatory mediators. To provide these active defense mechanisms, epithelial cells functionally express various pattern-recognition receptors. Toll-like receptors have been shown to recognize conserved microbial patterns mediating inducible activation of innate immunity. Mucosal surfaces, however, are prone to contact with pathogenic as well as non-pathogenic microbes and, therefore, immune-recognition principles have to be strictly regulated to avoid uncontrolled permanent activation. This review will focus on mechanisms by which epithelial cells regulate mucosal immune responses, thus creating an organ-specific microenvironment. This includes local adaptations in microbial recognition, regulation of local immune homeostasis, and modulation of antigen-presenting cells and adaptive immune responses. These regulatory mechanisms serve the special needs of controlled microbial recognition in mucosal compartments.
4

Evaluation of selected peripheral blood leukocyte functions in patients with various forms of periodontal disease

80%
Pietruska M., Zak J., Wysocka J., Jaworowska B., Zelazowska B., Lipska A., Stokowska W.
Archivum Immunologiae et Therapiae Experimentalis
|
2004
|
vol. 52
|
issue 3
208-212
EN
Periodontitis (P) is an infectious disease that develops in the supporting tissues of the tooth. One of the risk factors leading to it may be dysfunction of some immune system cells. Therefore, the object of the study was to assess selected functions of peripheral blood leukocytes in patients with various forms of P. As leukocytes are able to secrete interleukin (IL)-4 and IL-6, concentrations of their soluble receptors and the expression of their membrane receptors were investigated. Twenty generally healthy subjects with agressive (AP) and chronic periodontitis (CP) were enrolled in the study. The control group consisted of 8 healthy subjects, with no changes in periodontium. Peripheral blood mononuclear cells (PBMCs) were isolated and cultured. Levels of IL-4, IL-6, and their soluble receptors sIL-4R and sIL-6R were determined in the supernatant by ELISA. The expressions of cell surface IL-4R and IL-6R were assayed on PBMC using flow cytometry. No statistically significant differences were found in the selected parameters between people with periodontal disease and healthy controls. However, in subjects with AP, there was an increasing tendency in IL-6 concentration and IL-4R expression on PBMCs. Our results show that leukocytes play a significant part in P and their activity is probably lesion-dependent. Estimation of the cytokines secreted by leukocytes may facilitate differentiation and prognosis of the disease progression.
5
Content available remote

Pro-inflammatory cytokine TNF-alpha as a neuroprotective agent in the brain

80%
Figiel I.
Acta Neurobiologiae Experimentalis
|
2008
|
vol. 68
|
issue 4
526-534
EN
Despite the numerous reports on the role of tumor necrosis factor-alpha (TNF-alpha) in the brain neuropathology, very little is known about the mechanisms by which TNF-alpha may mediate neuroprotection. Different hypotheses pertain to the molecular and cellular effectors triggered by the activation of TNF receptors (TNFRI and TNFR2). They are focused on diminishing the production of nitric oxide and free radicals, alteration of excitatory amino acids neurotransmission, maintenance of neuronal calcium homeostasis and induction of neurotrophic factors synthesis. In this review all these data are summarized. Moreover, possible explanations for the inconsistent data concerning the TNF-alpha effect on neuron are discussed.
6

Enhancing cytotoxic t cell responses with altered-peptide ligands

80%
Zhao R., Collins E. J.
Archivum Immunologiae et Therapiae Experimentalis
|
2001
|
vol. 49
|
issue 4
271-278
EN
Interest in class I MHC-mediated immunotherapy is growing rapidly. In order to fight a virus or cancer effectively, a successful immunotherapeutic must activate a large number of specific CD8+ T cells and also generate immunological memory. Attempts to generate immune responses towards tumor- or virus-derived peptides have frequently been frustrated by the nature of the peptide antigen itself. Either the peptide does not bind well to its cognate MHC, or the T cells directed towards it have been functionally inactivated in vivo. Altered-peptide ligands are an effective way to circumvent these problems. However, generating enhanced binding of altered peptides to class I MHC while still maintaining recognition of the wild-type peptide is not straightforward. Many groups design enhanced binding peptides by substituting the observed anchor residues with those that are most preferred by the class I MHC molecule. For many antigenic peptides, this approach does not work. Furthermore, if a higher affinity peptide is designed, the substitutions may result in reduced recognition by CD8+ T cells. Therefore, the design of an altered-peptide ligand requires careful testing of each candidate therapeutic in terms of affinity for class I MHC and immunological reactivity. Lastly, immunotherapy using class I MHC must also take into account the large genetic heterogeneity in the population. A therapeutic that is only effective for 5-10 percent of the population is not as attractive as one that works for over 90% of the population. The use of MHC supertypes (groups of class I MHC allotypes that share similar peptide-binding characteristics) shows great promise in overcoming this problem.
7

Ligand-independent activity of the B cell antigen receptor in physiology and pathology

80%
Corcos D.
|
2007
|
vol. 55
|
issue 2
77-82
EN
The B cell receptor (BCR) is required for stimulation of B cells by antigen, and is also involved in the negative selection of autoreactive B cells. In the past few years, a constitutive ligand-independent signaling activity of the BCR has been demonstrated. In this paper, the various findings are summarized and their interpretation and their significance, both in pathology and in physiology discussed. The constitutive activity of the BCR may be important for tumor formation, at least in the case of heavy-chain diseases, neoplastic proliferations developed from B cells. A large body of evidence suggests that this activity could be required for B cell survival and would play a role in B cell development as a process monitoring BCR functionality. A model explaining signaling in the absence of antigen as a function of dimer formation is proposed. The putative constitutive activity of the pre-BCR is also discussed.
8
Content available remote

Expression of Angiopoietin-1 and the receptor Tie-2 mRNA in rat brains following intracerebral hemorrhage

80%
Zhou H. J., Tang T., Guo C., Zhang H. N., Zhong J. H., Zheng J., Luo J. K., Lin Y., Liu W., Luo W. F., Yang Q. D.
Acta Neurobiologiae Experimentalis
|
2008
|
vol. 68
|
issue 2
147-154
EN
Angiopoietin-1 (Ang-1) belongs to a novel family of endothelial growth factors that function as ligands for an endothelialspecific receptor tyrosine kinase (Tie-2). The Ang-1/Tie-2 system may contribute to angiogenesis and vascular remodeling by mediating interactions of endothelial cells with smooth muscle cells and pericytes. The spatial distribution and temporal expression of Ang-1 and Tie-2 in the rat brain were studied following collagenase-induced intracerebral hemorrhage (ICH), by immunohistochemistry and reverse transcription-polymerase chain (RT-PCR) analysis, respectively. Immunohistochemical analysis revealed that some Ang-1 or Tie-2-positive dilated vessels resided around the hematoma and extended into the clot. RT-PCR analysis showed that Ang-1 and Tie-2 mRNA signal was detected at 2 days and persisted for 28 days after ICH. These findings suggest that ICH could lead to upregulation of Ang-1 and the receptor Tie-2 mRNA.
9

Contribution of interleukin 2 and interleukin 12 receptors in signal transduction

80%
Lyszkiewicz M., Pajtasz-Piasecka E.
Postępy Higieny i Medycyny Doświadczalnej
|
2002
|
vol. 56
|
issue 6
707-731
EN
Interleukin 2 (IL-2) and interleukin 12 (IL-12) belong to lympho-hematopoietic cytokines and play a critical role in the promotion and enhancement of cellular response. IL-2 as the second signal of antigenic stimulation facilitates the transition of the cell cycle from phase G1 to phase S and is responsible for the regulation of T lymphocytes proliferation and the activation of cytotoxic T cells, natural killers, macrophages and granulocytes. IL-12 is the dominant factor in T helper cells polarization leading to the secretion of IFN-. Receptors for both of the cytokines (IL-2R or IL-12R) represent class I cytokine receptors composed of multiple subunits. Generally, they contain a similar extracellular conserved motif of four cysteines, and amino acid sequence - WSXWS (interacting directly with ligand) but possess no catalytic domens in the intrinsic tail of the chains. For this reason, to transfer the impact, the association with number of signaling molecules, allowing the activation of the signaling pathways is required. The connections of IL-2R or IL-12R with their ligands recruit receptor-associated cytoplasmic proteins from the JAK family (JAK1/JAK3 or JAK2/TYK2, respectively), which catalyze the phosphorylation of themselves and intrinsic tyrosine residues on the receptor, creating STAT docking sites. This phosphorylated and subsequent dimerised proteins bind rapidly to DNA and activate it. This review, presents the differences and similarities between the signaling pathways triggered by IL-2R or IL-12R ligation.
10

Toll-like receptor expression and function in airway epithelial cells

80%
Greene C. M., McElvaney N. G.
Archivum Immunologiae et Therapiae Experimentalis
|
2005
|
vol. 53
|
issue 5
418-427
EN
Toll-like receptors (TLRs) belong to a family of transmembrane proteins that can recognize and discriminate a diverse array of microbial antigens. Following their activation by specific ligands, TLRs initiate intracellular signaling cascades that culminate in the activation of transcription factors and ultimately lead to changes in pro-inflammatory gene expression. The TLR family constitutes an important component of the innate immune system and, although most commonly considered to be associated with immune cell responses, TLRs are also known to be functionally expressed on a variety of other cell types. Epithelial cells represent a significant component of the cellular content of the airways. These cells provide both a barrier to infection and an active defense mechanism against invading microbes. The expression and function of TLRs on airway epithelial cells has been an area of increasing interest in the recent past. This review will summarize advances in our understanding of the role of TLRs in airway epithelial cells.
11

Recent discoveries in the genetics of melanoma and their therapeutic implications

80%
Marquette A., Bagot M., Bensussan A., Dumaz N.
|
2007
|
vol. 55
|
issue 6
363-372
EN
The incidence of cutaneous malignant melanoma, tumors arising from melanocytes, has increased markedly over the past few years in many countries. Although early melanoma is curable through surgical excision, the prognosis of advanced melanoma is very poor, this tumor being resistant to current therapies. Thus there is a need for new therapies to improve the treatment of advanced melanoma. This review provides an overview of recent discoveries in the genetics of melanoma which could offer new therapeutic opportunities.
12

Leucine-rich repeats in host-pathogen interactions

80%
Kedzierski J., Montgomery J., Curtis J., Handman E.
|
EN
Leucine-rich repeats (LRRs) are versatile binding motifs found in a variety of proteins and are involved in protein-protein interactions. The LRR domain is composed of repeats forming a characteristic solenoid horse-shoe structure, which provides a scaffold for numerous insertions involved in binding to pathogen-associated molecular patterns and surface receptors. LRRs have been shown to be involved in the host defense systems of both plants (resistance genes) and mammals (Toll-like receptors and nucleotide-binding oligomerisation domain proteins), where they sense specific pathogen-associated molecules and activate the innate immune system. Paradoxically, LRRs have also been shown to be part of microbial virulence factors involved in the interaction with host cells and establishment of infection. The potential of LRRs to bind a vast array of structurally unrelated ligands and their well-documented involvement in microbial pathogenesis make them a potential target for vaccines and new drugs. The recent identification of LRRs in the obligate intracellular protozoan parasite Leishmania and their participation in the macrophage-parasite interaction have added new insight into the role of LRRs in the host cell invasion.
13

Recent advances in understanding of the molecular basis of anhidrotic ectodermal dysplasia: discovery of a ligand, ectodysplasin A and its two receptors

80%
Wisniewski S. A., Kobielak A., Trzeciak W. H., Kobielak K.
Journal of Applied Genetics
|
2002
|
vol. 43
|
issue 1
97-107
EN
Recent developments of the investigations on the molecular basis of anhidrotic ectodermal dysplasia are reviewed. Identification of the major product of the EDA gene (ectodysplasin A), a protein belonging to a group of TNF ligands, and molecular cloning of the cDNA, encoding its receptor (EDAR), a member of the TNF receptor family, are presented. The role of an alternative EDA receptor, localised on the X chromosome (XEDAR) in the developmental control of the differentiation of skin appendages, is discussed. Recent findings have elucidated the cause of the autosomal forms of EDA, both dominant and recessive, and indicated an important role of a signal transduction pathway involving a protein product of the NEMO gene and the transcription factor NFkB in the differentiation of skin appendages.
14

Histamine receptor expression on peripheral blood lymphocytes is influenced by specific and nonspecific activation

80%
Zak-Nejmark T., Kraus-Filarska M., Malolepszy J., Jankowska R., Jutel M., Nowak I. A., Nadobna G.
|
|
vol. 48
|
issue 2
107-110
EN
Histamine is a physiological mediator which exerts both effector and regulatory functions through its receptors on various cells. The aim of the study was to investigate changes in histamine receptor expression on peripheral blood lymphocytes affected by stimulation with both specific and nonspecific stimuli. Lymphocytes were obtained from both healthy and allergic subjects. Cells were incubated with various allergens (mixed grass pollen, Lolium perenne, Dermatophagoides pteronyssinus 1, bee venom, phospholipase A2) and nonspecific (fMLP, PMA/ionomycin, LPS) stimuli. The percentage of histamine-binding cells was determined with a fluorescence microscope after incubation with histamine-fluorescein. In control subjects histamine binding after stimulation with allergens was not significantly changed. In contrast, in allergic subjects stimulation with specific allergens resulted in significantly increased histamine binding. Nonspecific stimulation caused increased histamine binding to lymphocytes in both allergic subjects and healthy controls. We conclude that specific and nonspecific activation of lymphocytes is associated with increased expression of histamine receptors.
15

The murine Ly49 family: form and function

80%
Makrigiannis A. P., Anderson S. K.
Archivum Immunologiae et Therapiae Experimentalis
|
2001
|
vol. 49
|
issue 1
47-50
EN
The activity of natural killer (NK) cells is regulated by surface receptors that recognize class I MHC. Murine NK cells express a large family of lectin-related receptors (Ly49s) to perform this function, while human NK cells utilize a separate group of proteins containing Ig-related domains (KIRs). Although these receptor families not structurally related, the Ly49 family appears to be the functional equivalent of human KIRs, since it uses similar signal transduction pathways for either activation or inhibition of NK cell function. Therefore, lessons learned from the study of the murine MHC class I receptor system may be relevant to human NK function. This review summarizes the current state of knowledge of the Ly49 family.
16

Interleukin 6, tumor necrosis factor alpha and their soluble receptors in the blood serum of patients with denture stomatitis and fungal infection

71%
Pietruski J. K., Pietruska M. D., Jablonska E., Sacha P., Zaremba M., Stokowska W.
|
|
vol. 48
|
issue 2
101-105
EN
Determinations of the blood serum levels of interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-alpha) and their soluble receptors (sIL-6R, sTNFR) in denture stomatitis patients (DS) were performed. Serum levels of interleukins and their soluble receptors were measured using the ELISA method. In all examined patients mycological diagnostics were conducted using API 20C AUX stripe tests and an automatic ATB machine. Results were compared with those of healthy denture weares (D), and controls (C). In DS patients, yeasts were isolated in 90. 9%, in D in 66. 7% of cases. The most often isolated species in both groups was Candida albicans. Mean concentrations of IL-6 and TNF-alpha were statistically significantly higher in D and D groups compared to controls. Mean concentrations of sIL-6R were similar in all groups; however, concentrations of sTNFR in both DS and D groups were significantly lower compared to controls. There were no correlations found between values of IL-6 and TNF-alpha nor between examined interleukins and their soluble receptors.
17

Structure of antibody and limphocytes of receptor T ? similarities and differences

71%
Madalinski K., Michalkiewicz M. J., Michalkiewicz J.
Biotechnologia
|
2001
|
issue 3
71-77
EN
In this paper the structure of molecules responsible for recognition of foreign antigen is given.
18

Recent advances in understanding how interleukin 13 signals are involved in the pathogenesis of bronchial asthma

71%
Izuhara K., Umeshita R., AkaiwaM., Shirakawa T., Deichmann K. A., Arima K., Yu B., Hamasaki N., Hopkin J. M.
|
|
vol. 48
|
issue 5
505-512
EN
The prevalence of allergic disease has dramatically increased in recent decades, especially in urban and industralized areas. Allergic disease are disorders of the immune system, the results of complex interactions among various genetic and environmetal factors. Among them, the important role of interleukin 13 (IL-13), a TH2-type cytokine, has recently emerged in the pathogenesis of bronchial asthma. Based on studies using mice, great attention has been paid to the direct effects of IL-13 on bronchial tissues. In this review, we describe recent advances in understanding the signal transduction mechanism of IL-13, the infolvement of IL-13 signal-related genes as genetic factors in the pathogenesis of bronchial asthma, and the expression of IL-13 receptor on bronchial tissues. We describe potential strategies for targeting IL-13 signals to improve allergic states.
19

Innate immunity: cells, receptors, and signaling pathways

71%
Blach-Olszewska Z.
Archivum Immunologiae et Therapiae Experimentalis
|
2005
|
vol. 53
|
issue 3
245-253
EN
Essential differences between the innate and acquired branches of immunity are described. These differences concern the detection system (receptors and pathogen structures) and the cells engaged in both systems as well as the effectory mechanisms. In contrast to those of the acquired system, receptors of the innate system, which developed during evolution, recognize unchanged structures on large groups of pathogens (e.g. lipopolysaccharide in Gram-negative bacteria). Two lineages, natural killer (NK) and dendritic cells (DCs), play important roles in the innate system. Phenotypic and functional differentiation is observed among NKs and DCs, so each of their sublineages plays a different role in the innate system. Every lineage of cells of the innate immune system express different stimulatory and sometimes also inhibitory receptors on their surfaces (e.g. NK cells). Among the stimulatory are Toll-like receptors (TLRs), mannose and scavenger receptors, and the stimulatory receptors of NK cells. All TLRs show similarity in structure and in the kind of molecules involved in intracellular signaling. The immune reactions of the innate system involve cytokine-dependent resistance of cells against infection with pathogen, production of cytokines (tumor necrosis factor, interferons, interleukins, chemokines) and MHC-independent killing. Although these reactions protect the host from invasion by microorganisms, they can also be responsible for significant tissue damage or may stimulate the development of autoimmunity. Therefore innate immunity must be under rigorous control. The possible regulatory mechanisms of innate immunity are discussed.
20

Molecular characterization of Polish patients with familial hypercholesterolemia: novel and recurrent LDLR mutations

71%
Chmara M., Wasag B., Zuk M., Kubalska J., Wegrzyn A., Bednarska-Makaruk M., Pronicka E., Wehr H., Defesche J. C., Rynkiewicz A., Limon J.
|
|
vol. 51
|
issue 1
95-106
EN
Autosomal dominant hypercholesterolemia (ADH) is caused by mutations in the genes coding for the low-density lipoprotein receptor (LDLR), apolipoprotein B-100 (APOB), or proprotein convertase subtilisin/kexin type 9 (PCSK9). In this study, a molecular analysis of LDLR and APOB was performed in a group of 378 unrelated ADH patients, to explore the mutation spectrum that causes hypercholesterolemia in Poland. All patients were clinically diagnosed with ADH according to a uniform protocol and internationally accepted WHO criteria. Mutational analysis included all exons, exon-intron boundaries and the promoter sequence of the LDLR, and a fragment of exon 26 of APOB. Additionally, the MLPA technique was applied to detect rearrangements within LDLR. In total, 100 sequence variations were identified in 234 (62%) patients. Within LDLR, 40 novel and 59 previously described sequence variations were detected. Of the 99 LDLR sequence variations, 71 may be pathogenic mutations. The most frequent LDLR alteration was a point mutation p.G592E detected in 38 (10%) patients, followed by duplication of exons 4?8 found in 16 individuals (4.2%). Twenty-five cases (6.6%) demonstrated the p.R3527Q mutation of APOB. Our findings imply that major rearrangements of the LDLR gene as well as 2 point mutations (p.G592E in LDLR and p.R3527Q in APOB) are frequent causes of ADH in Poland. However, the heterogeneity of LDLR mutations detected in the studied group confirms the requirement for complex molecular studies of Polish ADH patients.
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.