CCL5 protein, human OR C483024 Dotaz Zobrazit nápovědu
Cysteine-cysteine chemokine ligand 5 (CCL5) with immunoregulatory and inflammatory activities has an important role in granuloma formations that activates and stimulates T-cells and macrophages. Cysteine-cysteine chemokine receptor 5 (CCR5) is a chemokine receptor, which is important for migration of immune cells to site of infection. In the present study we investigated the possible association between CCL5 -403G/A (rs2107538), CCL5 -28C/G (rs2280788) and CCR5 Δ32 polymorphisms and pulmonary tuberculosis (PTB) in an Iranian population. This case-control study was performed on 160 patients with pulmonary tuberculosis and 160 unrelated healthy subjects. The CCL5 -403G/A, CCL5 -28C/G and CCR5 Δ32 polymorphisms were genotyped by allele-specific polymerase chain reaction (AS-PCR), tetra amplification refractory mutation system polymerase chain reaction (T-ARMS PCR) and PCR, respectively. Our results showed that GA as well as GA+AA genotypes of CCL5 -403G/A (rs2107538) increased the risk of PTB in comparison with GG genotype (OR=1.70, 95% CI=1.03-2.81, P=0.038 and OR=1.64, 95% CI=1.00-2.68, P=0.049, respectively). No significant association was found between CCL5 -28C/G as well as CCR5 Δ32 polymorphism and PTB risk. In conclusion, our findings proposed that CCL5 -403G>A polymorphism may be a risk factor for susceptibility to PTB in our population. Larger sample sizes with different ethnicities are required to validate our findings.
- Klíčová slova
- CCL5, CCR5, Polymorphism, Tuberculosis,
- MeSH
- chemokin CCL5 genetika MeSH
- dospělí MeSH
- genetická predispozice k nemoci genetika MeSH
- genotyp MeSH
- lidé středního věku MeSH
- lidé MeSH
- plicní tuberkulóza genetika MeSH
- polymerázová řetězová reakce MeSH
- polymorfismus délky restrikčních fragmentů * MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- srovnávací studie MeSH
- Geografické názvy
- Írán MeSH
- Názvy látek
- CCL5 protein, human MeSH Prohlížeč
- chemokin CCL5 MeSH
BACKGROUND: Chemokines and chemokine receptors are major mediators of leukocyte trafficking into the sites of the immune response. They participate in defence against microbial infection, in Th1/Th2 polarization of the immune response, allograft rejection and angiogenesis/angiostasis as well as in tumorigenesis and metastasis. To date, several functional polymorphisms of chemokine and chemokine receptor genes have been discovered that are able to deregulate chemokine system and, therefore, they may interfere with the pathogenesis of a large number of inflammatory and other diseases. In this review we focus on the known polymorphisms of two chemokines: CCL2, CCL5 and their corresponding receptors (CCR2, CCR5) and we also discuss their associations with susceptibility and progression to selected immune-mediated diseases. METHODS AND RESULTS: Based on relevant literature this article gives a short overview of case-control and family studies regarding effect of the genetic factors on diseases such as coronary artery disease, systemic lupus erythematosus, diabetes mellitus, lung diseases and others. CONCLUSION: Recent advance in the identification of chemokine genetic background of the diseases could provide opportunity for pharmacological treatment. However, we need more information about posttranscriptional events to understand functional relevance of polymorphisms and to discovery new avenues to blocking disease development.
- MeSH
- chemokin CCL2 genetika MeSH
- chemokin CCL5 genetika imunologie fyziologie MeSH
- lidé MeSH
- polymorfismus genetický * MeSH
- receptory CCR2 genetika imunologie fyziologie MeSH
- receptory CCR5 genetika imunologie fyziologie MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- přehledy MeSH
- Názvy látek
- chemokin CCL2 MeSH
- chemokin CCL5 MeSH
- receptory CCR2 MeSH
- receptory CCR5 MeSH
Coronary artery inflammation is a critical process in the pathogenesis of myocardial infarction (MI). The chemokine CCL5/RANTES (regulated upon activation, normal T cells expressed and secreted) is expressed in advanced atherosclerotic lesions. Functional polymorphisms of the RANTES gene can, therefore, be involved in the pathogenesis of coronary artery disease. We examined the association of polymorphisms in the RANTES gene with myocardial infarction in Slavonic populations of Czech and Russian origin. A total of 467 post-MI patients and 337 control subjects were genotyped for RANTES promoter G-403A (rs2107538) and intron 1.1 T/C (rs2280789) variants by PCR-SSP. Both RANTES genotypes and allele frequencies did not differ between case and control groups. Haplotype-based analysis also failed to reveal an association between MI and investigated markers. Strong linkage disequilibrium was detected between particular RANTES alleles. The data do not support an association between RANTES G-403A polymorphism and MI, as reported previously.
- MeSH
- běloši genetika MeSH
- chemokin CCL5 genetika imunologie MeSH
- dospělí MeSH
- genetická predispozice k nemoci MeSH
- genotyp MeSH
- infarkt myokardu genetika imunologie MeSH
- jednonukleotidový polymorfismus * MeSH
- lidé středního věku MeSH
- lidé MeSH
- nemoci koronárních tepen genetika MeSH
- promotorové oblasti (genetika) MeSH
- senioři MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Geografické názvy
- Česká republika MeSH
- Rusko MeSH
- Názvy látek
- chemokin CCL5 MeSH
The MCP-1/CCL2 as well as RANTES/CCL5 chemokines are potent chemoattractants involved in immunoregulatory and inflammatory processes of rheumatoid arthritis. Recent studies demonstrated elevated levels of MCP-1 and RANTES in plasma, synovial fluid, and the synovial tissue of patients with RA. To examine the relationship among MCP-1 and RANTES single nucleotide polymorphisms and circulating levels and rheumatoid arthritis (RA), a total of 156 RA patients and 125 controls were recruited into the study. An association of -855 C/G MCP-1 polymorphism to IgM RF within the RA patients was observed. The lowest circulating levels of RANTES were observed in the AA variant of RANTES -403 G/A polymorphism. Furthermore, an association of -403 AA variant to circulating levels of IL-15 and IL-10 was found. No associations of factors describing rheumatoid arthritis (RFs, ANA, anti-CCP-positive/negative, DAS 28 score and number of swollen joints) with MCP-1 levels, genotype distribution, allelic frequencies and/or frequencies of haplotypes composed of all three studied polymorphisms in promoter region of MCP-1, and RANTES polymorphism were observed. We conclude that the RANTES promoter polymorphism is associated to circulating levels of RANTES, IL15 and IL10. However, our findings suggest that polymorphisms in the MCP-1 and RANTES gene promoters do not contribute significantly to the interindividual RA susceptibility and/or severity in Caucasians.
- MeSH
- chemokin CCL2 krev genetika imunologie MeSH
- chemokin CCL5 krev genetika imunologie MeSH
- dospělí MeSH
- imunoglobulin M genetika imunologie MeSH
- interleukin-10 krev MeSH
- interleukin-15 krev MeSH
- jednonukleotidový polymorfismus MeSH
- lidé středního věku MeSH
- lidé MeSH
- mladý dospělý MeSH
- promotorové oblasti (genetika) MeSH
- revmatoidní artritida genetika imunologie MeSH
- senioři nad 80 let MeSH
- senioři MeSH
- synoviální membrána metabolismus MeSH
- synoviální tekutina metabolismus MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mladý dospělý MeSH
- mužské pohlaví MeSH
- senioři nad 80 let MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- CCL2 protein, human MeSH Prohlížeč
- CCL5 protein, human MeSH Prohlížeč
- chemokin CCL2 MeSH
- chemokin CCL5 MeSH
- imunoglobulin M MeSH
- interleukin-10 MeSH
- interleukin-15 MeSH
Acyclic nucleoside phosphonates are novel class of clinically broadly used antivirotics effective against replication of both DNA viruses and retroviruses including human immunodeficiency virus (HIV). We have investigated their in vitro effects on immune defence mechanisms in human peripheral blood mononuclear cells, with the main emphasis on expression of cytokines which are able to suppress the entry of HIV in cells. Included in the study were prototype acyclic nucleoside phosphonates, i.e. 9-[2-(phosphonomethoxy)ethyl]adenine (PMEA; adefovir), 9-[2-(phosphonomethoxy)ethyl]-2,6-diaminopurine (PMEDAP), (R)-and (S)-enantiomers of 9-[2-(phosphonomethoxy)propyl]adenine [(R)-PMPA; tenofovir] and [(S)-PMPA], and of 9-[2-(phosphonomethoxy)propyl]-2,6-diaminopurine [(R)-PMPDAP] and [(S)-PMPDAP], and their N(6)-substituted derivatives. Some of the compounds were found to substantially enhance secretion of chemokines such as macrophage inflammatory protein-1alpha (MIP-alpha/CCL3), and "regulated on activation of normal T cell expressed and secreted" (RANTES/CCL5). Secretion of MIP-1beta/CCL4 was only marginally increased, whereas production of interleukin-16 (IL-16) and interferon-gamma (IFN-gamma) remained uninfluenced. The most effective proved to be the N(6)-cyclooctyl-PMEDAP, N(6)-isobutyl-PMEDAP, N(6)-pyrrolidino-PMEDAP, N(6)-cyclopropyl-(R)-PMPDAP, and N(6)-cyclopentyl-(R)-PMPDAP derivatives. Remarkably enhanced secretion of chemokines was reached within 2-4 h of the cell culture, and was observed at concentration of 2-5 microM. It may be suggested that acyclic nucleoside phosphonates represent a new generation of antivirotics with combined antimetabolic and therapeutically prospective immunostimulatory properties.
- MeSH
- adenin analogy a deriváty chemie farmakologie MeSH
- analýza rozptylu MeSH
- antiretrovirové látky farmakologie MeSH
- chemokin CCL3 metabolismus MeSH
- chemokin CCL4 metabolismus MeSH
- chemokin CCL5 MeSH
- chemokiny metabolismus MeSH
- dospělí MeSH
- interferon gama metabolismus MeSH
- kultivované buňky MeSH
- leukocyty mononukleární účinky léků metabolismus MeSH
- lidé středního věku MeSH
- lidé MeSH
- organofosfonáty chemie farmakologie MeSH
- stereoizomerie MeSH
- vztahy mezi strukturou a aktivitou MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- adenin MeSH
- antiretrovirové látky MeSH
- CCL3 protein, human MeSH Prohlížeč
- CCL4 protein, human MeSH Prohlížeč
- chemokin CCL3 MeSH
- chemokin CCL4 MeSH
- chemokin CCL5 MeSH
- chemokiny MeSH
- interferon gama MeSH
- organofosfonáty MeSH
Transplantation of mesenchymal stem cells (MSC) improves functional recovery in experimental models of spinal cord injury (SCI); however, the mechanisms underlying this effect are not completely understood. We investigated the effect of intrathecal implantation of human MSC on functional recovery, astrogliosis and levels of inflammatory cytokines in rats using balloon-induced spinal cord compression lesions. Transplanted cells did not survive at the lesion site of the spinal cord; however, functional recovery was enhanced in the MSC-treated group as was confirmed by the Basso, Beattie, and Bresnahan (BBB) and the flat beam test. Morphometric analysis showed a significantly higher amount of remaining white matter in the cranial part of the lesioned spinal cords. Immunohistochemical analysis of the lesions indicated the rearrangement of the glial scar in MSC-treated animals. Real-time PCR analysis revealed an increased expression of Irf5, Mrc1, Fgf2, Gap43 and Gfap. Transplantation of MSCs into a lesioned spinal cord reduced TNFα, IL-4, IL-1β, IL-2, IL-6 and IL-12 and increased the levels of MIP-1α and RANTES when compared to saline-treated controls. Intrathecal implantation of MSCs reduces the inflammatory reaction and apoptosis, improves functional recovery and modulates glial scar formation after SCI, regardless of cell survival. Therefore, repeated applications may prolong the beneficial effects induced by MSC application.
- MeSH
- chemokin CCL5 genetika metabolismus MeSH
- fibroblastový růstový faktor 2 genetika metabolismus MeSH
- gliový fibrilární kyselý protein genetika metabolismus MeSH
- interferonové regulační faktory genetika metabolismus MeSH
- interleukiny genetika metabolismus MeSH
- krysa rodu Rattus MeSH
- lidé MeSH
- lokomoce MeSH
- mezenchymální kmenové buňky metabolismus MeSH
- poranění míchy metabolismus terapie MeSH
- potkani Wistar MeSH
- protein GAP-43 genetika metabolismus MeSH
- receptory imunologické genetika metabolismus MeSH
- TNF-alfa genetika metabolismus MeSH
- transplantace mezenchymálních kmenových buněk * MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- lidé MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- chemokin CCL5 MeSH
- fibroblastový růstový faktor 2 MeSH
- gliový fibrilární kyselý protein MeSH
- interferonové regulační faktory MeSH
- interleukiny MeSH
- protein GAP-43 MeSH
- receptory imunologické MeSH
- TNF-alfa MeSH
BACKGROUND: CC chemokine ligand (CCL)5 and its receptor CCR5 contribute to leukocyte migration into lungs of patients with diffuse lung diseases (DLD). Pharmacological regulation of CCL5 and CCR5 expression was therefore explored in bronchoalveolar cells obtained from patients with DLD. METHODS: Cells from 21 patients were co-cultivated in vitro with tumour necrosis factor-alpha and dexamethasone, cyclosporin A (CyA) or pentoxifylline. Chemokine mRNA expression and protein production was assessed by reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. RESULTS: Dexamethasone altered CCL5 mRNA expression and suppressed its protein levels. CyA inhibited chemokine mRNA expression but not protein production. Pentoxifylline did not affected chemokine expression. Both dexamethasone and CyA suppressed CCR5 mRNA transcripts. CONCLUSION: In conclusion, while dexamethasone downregulates the CCL5 functional form, CyA and pentoxifylline have no effects on CCL5 protein. These data provide in vitro correlation for clinical applications of immunomodulators in therapy of DLD.
- MeSH
- bronchoalveolární lavážní tekutina cytologie MeSH
- chemokin CCL5 MeSH
- chemokiny CC genetika metabolismus MeSH
- cyklosporin farmakologie MeSH
- dexamethason farmakologie MeSH
- dospělí MeSH
- glukokortikoidy farmakologie MeSH
- imunosupresiva farmakologie MeSH
- inhibitory enzymů farmakologie MeSH
- kultivované buňky MeSH
- leukocyty cytologie účinky léků imunologie metabolismus MeSH
- lidé středního věku MeSH
- lidé MeSH
- messenger RNA metabolismus MeSH
- pentoxifylin farmakologie MeSH
- plicní nemoci metabolismus patologie MeSH
- receptory CCR5 genetika metabolismus MeSH
- senioři MeSH
- TNF-alfa farmakologie MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- CCL5 protein, human MeSH Prohlížeč
- chemokin CCL5 MeSH
- chemokiny CC MeSH
- cyklosporin MeSH
- dexamethason MeSH
- glukokortikoidy MeSH
- imunosupresiva MeSH
- inhibitory enzymů MeSH
- messenger RNA MeSH
- pentoxifylin MeSH
- receptory CCR5 MeSH
- TNF-alfa MeSH
BACKGROUND: Our study focused on the ability of epicardial adipocytes to produce bioactive substances and compare the extent of this production with the production of adipokines in visceral adipocytes, which are well known endocrine cells capable of contributing to the development of atherosclerosis. MATERIAL AND METHODS: The gene expression of human cytokines (IL-6, IL-8, IL-18, RANTES and MCP-1) and adipokines (leptin and adiponectin) was measured in primary cell lines of epicardial and visceral adipocytes, both in undifferentiated and mature statuses, after a 21-day-long differentiation protocol. Each condition was assayed in triplicate in two independent primary cell lines obtained from two different donors. RESULTS: The epicardial preadipocytes showed an increased expression of IL-8 (3.25-fold, p<0.05) compared with visceral preadipocytes. The expression of the atheroprotective adiponectin in epicardial preadipocytes was minimal compared with the expression in visceral preadipocytes (p<0.0001). Moreover, the expression of the genes of interest was dependent on the differentiation degree and cell origin. We observed an altered expression of the proinflammatory genes IL-8 (0.016-fold, p<0.01) and MCP-1 (0.19-fold, p<0.05) in differentiated epicardial adipocytes compared with undifferentiated adipocytes. The epicardial adipocytes showed an increased expression of IL-6 (8.13-fold, p<0.05) compared with the visceral adipocytes. CONCLUSION: Our results suggest that epicardial adipocytes substantially differ from visceral adipocytes and might locally contribute to the pathogenesis of coronary atherosclerosis.
- MeSH
- buněčná diferenciace fyziologie MeSH
- chemokin CCL2 genetika MeSH
- chemokin CCL5 genetika MeSH
- cytokiny genetika MeSH
- dospělí MeSH
- exprese genu fyziologie MeSH
- interleukin-18 genetika MeSH
- interleukin-6 genetika MeSH
- interleukin-8 genetika MeSH
- kultivované buňky MeSH
- lidé MeSH
- nitrobřišní tuk cytologie fyziologie MeSH
- perikard cytologie fyziologie MeSH
- pilotní projekty MeSH
- tukové buňky cytologie fyziologie MeSH
- Check Tag
- dospělí MeSH
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- srovnávací studie MeSH
- Názvy látek
- CCL2 protein, human MeSH Prohlížeč
- CCL5 protein, human MeSH Prohlížeč
- chemokin CCL2 MeSH
- chemokin CCL5 MeSH
- CXCL8 protein, human MeSH Prohlížeč
- cytokiny MeSH
- IL6 protein, human MeSH Prohlížeč
- interleukin-18 MeSH
- interleukin-6 MeSH
- interleukin-8 MeSH
Upregulation of genes for interferon (IFN)-γ and CXC chemokine receptor (CXCR)3 expression, two crucial molecules in sarcoid inflammation and granuloma formation, is directly controlled by the T-helper (Th)1 transcription factor T-bet (T-box, expressed in T-cells). However, there is no information on T-bet expression in sarcoidosis or its relationship with "sarcoidosis-associated" genes. Therefore, we investigated expression of T-bet mRNA and, in parallel, a spectrum of genes known to be involved in sarcoidosis pathogenesis. Transcripts were determined in bronchoalveolar lavage (BAL) cells from 62 sarcoidosis patients and 25 controls by quantitative RT-PCR; T-bet protein was localised by immunohistochemistry. Patient's BAL cells expressed higher mRNA T-bet levels than those of controls (mean ± sd fold change 3.64 ± 1.72; p = 0.00006). T-bet mRNA expression did not vary between clinical phenotypes as assessed by chest radiography stage, presence/absence of Löfgren's syndrome, extrapulmonary/pulmonary involvement or progressing/remitting disease (p > 0.05). T-bet mRNA expression correlated with expression of IFN-γ, CC chemokine ligand 5, CXC chemokine ligand (CXC)10, interleukin (IL)-2 receptor/IL-15 receptor β, CXCR3 and CXCR6 (p < 0.01). T-bet protein was localised to alveolar macrophages and lymphocytes, tissue multinucleated giant cells, macrophages and lymphocytes. In pulmonary sarcoidosis, T-bet upregulation is associated with changes in expression of IFN-γ, CXCR3 and chemokines/receptors involved in the pathogenesis of sarcoidosis, which suggests a role for T-bet in this Th1 disease, including modulation of some sarcoidosis-associated genes.
- MeSH
- bronchoalveolární lavážní tekutina chemie cytologie MeSH
- chemokin CCL5 genetika metabolismus MeSH
- dospělí MeSH
- exprese genu MeSH
- interferon gama genetika metabolismus MeSH
- lidé středního věku MeSH
- lidé MeSH
- lymfatické uzliny metabolismus MeSH
- messenger RNA metabolismus MeSH
- plíce metabolismus MeSH
- plicní sarkoidóza genetika imunologie metabolismus MeSH
- proteiny T-boxu metabolismus MeSH
- receptory chemokinů genetika metabolismus MeSH
- receptory CXCR3 genetika metabolismus MeSH
- receptory CXCR6 MeSH
- receptory interleukinu-2 genetika metabolismus MeSH
- Th1 buňky imunologie metabolismus MeSH
- upregulace * MeSH
- virové receptory genetika metabolismus MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- CCL5 protein, human MeSH Prohlížeč
- chemokin CCL5 MeSH
- CXCR6 protein, human MeSH Prohlížeč
- interferon gama MeSH
- messenger RNA MeSH
- proteiny T-boxu MeSH
- receptory chemokinů MeSH
- receptory CXCR3 MeSH
- receptory CXCR6 MeSH
- receptory interleukinu-2 MeSH
- T-box transcription factor TBX21 MeSH Prohlížeč
- virové receptory MeSH
Despite advances in immunosuppression in past decades, allograft rejection remains the main reason for kidney graft failure. Recently, despite great improvements in understanding of molecular basis of allograft rejections, renal histology remains the primary method to monitor the onset of graft rejection. The aim of the present study was to ascertain whether cytokine and chemokine expression profiles in kidney allografts contributed to the diagnosis of graft dysfunction. We analyzed mRNA expression in 174 kidney graft biopsies for the following cytokines: TGF-beta1, TNF-alpha, IL-10, and chemokine RANTES. Based on the expression levels obtained by real-time RT-PCR, we correlated data with the results of morphologic examinations. All tested cytokines and chemokines were upregulated (P < .001) during acute rejection compared to nonrejecting controls. Upregulation was also found in chronic allograft nephropathy (CAN) group for TGF-beta1, IL-10 (P < .001), TNF-alpha, and RANTES (P < .01). Upregulated expression of IL-10 (P < .001), TGF-beta1, (P < .01) and RANTES (P < .05) showed borderline changes. Higher expression levels (P < .001) of TGF-beta1 and IL-10 were also found during ATN. IL-10 was upregulated (P < .01) in specimens with recurrent glomerulonephritis. Weakly increased (P < .05) expressions of TGF-beta1 were found during CsA toxicity. Distinctive expression levels between acute rejection and CAN were only found for IL-10 (P < .01). TNF-alpha showed a different expression profile in acute rejection versus ATN (P < .001). These findings suggest that distinct cytokine and chemokine expression profiles in grafts may contribute to the diagnosis for and elucidation of the immunopathologic process during graft dysfunction.
- MeSH
- časové faktory MeSH
- chemokin CCL5 genetika MeSH
- chemokiny genetika MeSH
- cytokiny genetika MeSH
- genetická transkripce imunologie MeSH
- interleukin-10 genetika MeSH
- lidé MeSH
- messenger RNA genetika MeSH
- polymerázová řetězová reakce s reverzní transkripcí MeSH
- regulace genové exprese imunologie MeSH
- rejekce štěpu patologie MeSH
- TNF-alfa genetika MeSH
- transformující růstový faktor beta genetika MeSH
- transformující růstový faktor beta1 MeSH
- transplantace ledvin imunologie patologie MeSH
- Check Tag
- lidé MeSH
- mužské pohlaví MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- chemokin CCL5 MeSH
- chemokiny MeSH
- cytokiny MeSH
- interleukin-10 MeSH
- messenger RNA MeSH
- TGFB1 protein, human MeSH Prohlížeč
- TNF-alfa MeSH
- transformující růstový faktor beta MeSH
- transformující růstový faktor beta1 MeSH