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1.
Clin Transl Gastroenterol ; 9(10): 201, 2018 11 02.
Artículo en Inglés | MEDLINE | ID: mdl-30385752

RESUMEN

OBJECTIVE: Immune dysregulation, polyendocrinopathy, enteropathy, X-linked (IPEX) syndrome is an autoimmune disease caused by mutations in the forkhead box protein 3 gene (FOXP3), which encodes a key regulator of immune tolerance. The aim of this study was to describe the clinical heterogeneity of the disease in a national French cohort. METHODS: Multicenter retrospective study of patients diagnosed with IPEX syndrome caused by mutations in FOXP3. RESULTS: Thirty children from 26 families were included. Age at disease onset (median [first to third quartile]) was 1.5 mo [0-84] and at death 3.5 years [0-10.5] (n = 15) indicating a high heterogeneity. Initial presentation was diarrhoea (68%), type 1 diabetes (T1D; 25%), skin lesions (7%) and nephropathy (3%). During the course of the disease the following main symptoms were observed: diarrhoea (100%), skin lesions (85%), T1DM (50%), severe food allergies (39%), haematological disorders (28%), nephropathies (25%), hepatitis (14%) as well as the presence of a variety of autoantibodies. Immunosuppressive mono- or combination therapy led to improvement in eight children. Three boys displayed a stable disease course without any immunosuppressive medication. Overall 10-year survival rate was 43% (42% in transplanted patients and 52% in patients on immunosuppressive therapy). Five out of 22 identified FOXP3 mutations have not been described yet: c.-23 + 1G > A, c.-23 + 5G > A, c.264delC, c.1015C > T and c.1091A > G. The first two produced atypical, attenuated phenotypes. Missense and frameshift mutations affecting the forkhead domain were associated with poor survival (Gehan-Wilcoxon p = 0.002). CONCLUSION: The broad phenotypic heterogeneity of IPEX raises questions about modifying factors and justifies early FOXP3 sequencing in suspected cases.


Asunto(s)
Factores de Transcripción Forkhead/genética , Enfermedades Genéticas Ligadas al Cromosoma X/genética , Enfermedades Intestinales/genética , Poliendocrinopatías Autoinmunes/genética , Autoanticuerpos/sangre , Variación Biológica Poblacional , Niño , Preescolar , Diabetes Mellitus Tipo 1/genética , Diarrea/genética , Factores de Transcripción Forkhead/inmunología , Francia , Enfermedades Genéticas Ligadas al Cromosoma X/inmunología , Enfermedades Genéticas Ligadas al Cromosoma X/terapia , Humanos , Terapia de Inmunosupresión , Lactante , Recién Nacido , Enfermedades Intestinales/inmunología , Enfermedades Intestinales/terapia , Enfermedades Renales/genética , Masculino , Mutación , Poliendocrinopatías Autoinmunes/inmunología , Poliendocrinopatías Autoinmunes/terapia , Estudios Retrospectivos , Enfermedades Cutáneas Genéticas/genética , Tasa de Supervivencia , Síndrome
2.
Arch Pediatr ; 2018 Jun 16.
Artículo en Inglés | MEDLINE | ID: mdl-29921470

RESUMEN

TTC7A mutations cause multiple neonatal intestinal atresias with early inflammatory bowel disease and severe combined immunodeficiency. There are no treatment protocols for this rare disease. Two new cases are described for which radical early treatment measures - total enterectomy, home parenteral nutrition, immunoglobulin therapy and intravenous antibiotic prophylaxis - have allowed both patients to develop optimally.

3.
J Intern Med ; 274(4): 351-62, 2013 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-23772771

RESUMEN

OBJECTIVE: Hereditary haemorrhagic telangiectasia (HHT) is a genetic disorder related to mutations in one of the coreceptors to the transforming growth factor-ß superfamily (ALK1 or endoglin). Besides the obvious vascular symptoms (epistaxis and arteriovenous malformations), patients have an unexplained high risk of severe bacterial infections. The aim of the study was to assess the main immunological functions of patients with HHT using the standard biological tests for primary immunodeficiencies. DESIGN, SETTING AND SUBJECTS: A prospective single-centre study of 42 consecutive adult patients with an established diagnosis of HHT was conducted at the National French HHT Reference Center (Lyon). Lymphocyte subpopulations and proliferation capacity, immunoglobulin levels and neutrophil and monocyte phagocytosis, oxidative burst and chemotaxis were assessed. RESULTS: Innate immunity was not altered in patients with HHT. With regard to adaptive immunity, significant changes were seen in immunological parameters: primarily, a lymphopenia in patients with HHT compared with healthy control subjects affecting mean CD4 (642 cells µL(-1) vs. 832 cells µL(-1) , P < 0.001), CD8 (295 cells µL(-1) vs. 501 cells µL(-1) , P < 0.0001) and natural killer (NK) cells (169 cells µL(-1) vs. 221 cells µL(-1) , P < 0.01), associated with increased levels of immunoglobulins G and A. This lymphopenia mainly concerned naïve T cells. Proliferation capacities of lymphocytes were normal. Lymphopenic patients had a higher frequency of iron supplementation but no increase in infection rate. Lower levels of immunoglobulin M and a higher rate of pulmonary arteriovenous malformations were found amongst patients with a history of severe infection. CONCLUSIONS: Patients with HHT exhibit immunological abnormalities including T CD4, T CD8 and NK cell lymphopenia and increased levels of immunoglobulins G and A. The observed low level of immunoglobulin M requires further investigation to determine whether it is a specific risk factor for infection in HHT.


Asunto(s)
Linfocitos T CD4-Positivos/inmunología , Linfocitos T CD8-positivos/inmunología , Hipergammaglobulinemia/etiología , Linfopenia/etiología , Telangiectasia Hemorrágica Hereditaria/complicaciones , Adulto , Anciano , Anciano de 80 o más Años , Femenino , Humanos , Hipergammaglobulinemia/inmunología , Inmunidad Innata/genética , Inmunoglobulina A/inmunología , Inmunoglobulina G/inmunología , Linfopenia/inmunología , Masculino , Persona de Mediana Edad , Estudios Prospectivos , Factores de Riesgo , Telangiectasia Hemorrágica Hereditaria/genética , Telangiectasia Hemorrágica Hereditaria/inmunología , Adulto Joven
4.
Transplant Proc ; 41(8): 3347-52, 2009 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-19857747

RESUMEN

OBJECTIVES: The use of mesenchymal stem cells (MSC), which display immunosuppressive activity, seems to be a promising therapeutic approach in solid organ transplantation. However, little is known about their interactions with immunosuppressive drugs. The objective of this study was to assess these interactions in allogeneic responses. METHODS: We studied the effects on alloimmune responses in mixed lymphocyte reactions of MSC plus five agents-cyclosporine, tacrolimus, rapamycin, mycophenolate acid (MPA), and dexamethasone (DEX). RESULTS: Human MSC isolated from bone marrow were characterized by their phenotype and their ability to differentiate into adipocytes or osteoblastes. MSC plus the agents inhibited allogeneic lymphocyte proliferation in a dose-dependent manner. Calcineurin inhibitors and rapamycin antagonized the inhibitory effect of MSC, whereas MPA promoted it and DXM did not modify it. CONCLUSION: MPA seems to be the best immunosuppressant to associated with MSC for transplanted patients.


Asunto(s)
Inmunosupresores/farmacología , Células Madre Mesenquimatosas/inmunología , Trasplante Homólogo/inmunología , Adipocitos/efectos de los fármacos , Adipocitos/inmunología , Antígenos CD/inmunología , Células de la Médula Ósea/citología , Células de la Médula Ósea/efectos de los fármacos , Células de la Médula Ósea/inmunología , Diferenciación Celular , Ciclosporina/farmacología , Dexametasona/farmacología , Citometría de Flujo , Humanos , Linfocitos/efectos de los fármacos , Linfocitos/inmunología , Células Madre Mesenquimatosas/efectos de los fármacos , Ácido Micofenólico/farmacología , Osteoblastos/efectos de los fármacos , Osteoblastos/inmunología , Sirolimus/farmacología
6.
FASEB J ; 20(12): 2081-92, 2006 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-17012260

RESUMEN

Recent evidence indicates that microglial cells may not derive from blood circulating mature monocytes as they express features of myeloid progenitors. Here, we observed that a subpopulation of microglial cells expressed CD34 and B220 antigens during brain development. We thus hypothesized that microglia, or a subset of microglial cells, originate from blood circulating CD34+/B220+ myeloid progenitors, which could target the brain under developmental or neuroinflammatory conditions. Using experimental allergic encephalomyelitis (EAE) as a model of chronic neuroinflammation, we found that a discrete population of CD34+/B220+ cells expands in both blood and brain of diseased animals. In EAE mice, intravenous transfer experiments showed that macrophage-colony stimulating factor (M-CSF) -expanded CD34+ myeloid progenitors target the inflamed central nervous system (CNS) while keeping their immature phenotype. Based on these results, we then assessed whether CD34+/B220+ cells display in vitro differentiation potential toward microglia. For this purpose, CD34+/B220+ cells were sorted from M-CSF-stimulated bone marrow (BM) cultures and exposed to a glial cell conditioned medium. Under these experimental conditions, CD34+/B220+ cells were able to differentiate into microglial-like cells showing the morphological and phenotypic features of native microglia. Overall, our data suggest that under developmental or neuroinflammatory conditions, a subpopulation of microglial cells derive from CNS-invading CD34+/B220+ myeloid progenitors.


Asunto(s)
Encéfalo , Diferenciación Celular , Células Madre Hematopoyéticas/citología , Células Madre Hematopoyéticas/fisiología , Inflamación/patología , Microglía/citología , Animales , Animales Recién Nacidos , Antígenos CD34 , Células de la Médula Ósea , Encéfalo/crecimiento & desarrollo , Encéfalo/patología , Linaje de la Célula , Movimiento Celular , Encefalomielitis Autoinmune Experimental/patología , Femenino , Antígenos Comunes de Leucocito , Ratones , Ratones Endogámicos C57BL
7.
Rev Med Interne ; 26(2): 95-102, 2005 Feb.
Artículo en Francés | MEDLINE | ID: mdl-15710255

RESUMEN

PURPOSE: Autoimmune manifestations (AIM) are associated to common variable immunodeficiency (CVI) in about 20 to 25% of the cases. This study presents the clinical, biological characteristics and the evolution of nine patients developing CVI and AIM. A peripheral B-cell compartment analysis has been performed in seven cases. METHOD: This multicenter retrospective study analyses nine patients, six men and three women, within a population of 32 CVI. RESULTS: The mean age was 27 years at the time of diagnosis of AIM and 30 years at the time of diagnosis of CVI. The diagnosis of AIM preceded the diagnosis of CVI in five cases. Thirteen AIM of different types were observed: autoimmune hemolytic anemia (AHA, 3), immune thrombocytopenic purpura (ITP, 2), Evan's syndrome (2), primary biliary cirrhosis (1), rheumatoid arthritis (1), alopecia totalis (1), myasthenia gravis (1). The peripheral B-cell compartment was investigated in seven patients: five patients with autoimmune cytopenia presented with a diminution of memory B cells (CD27+IgD-) and immature B cells (CD21-) levels; the patient with primary biliary cirrhosis and myasthenia gravis had only a diminution of memory B cells level; the last patient with ITP presented with a normal level of memory B cells. Five among the seven patients with autoimmune cytopenia required a specific treatment using corticosteroids, high dosages of intravenous immunoglobulin, then splenectomy after failure of the medical management, with severe infectious complications in one case. CONCLUSION: The association of AIM and CVI is not fortuitous. The most common AIM is autoimmune cytopenia. The peripheral B-cell compartment analyses show that a majority of patients have a defect in memory B-cells. Treatment regimens are not standardized and splenectomy increases the risk of infectious complications.


Asunto(s)
Enfermedades Autoinmunes/complicaciones , Inmunodeficiencia Variable Común/complicaciones , Adolescente , Corticoesteroides/uso terapéutico , Adulto , Factores de Edad , Alopecia/complicaciones , Alopecia/inmunología , Anemia Hemolítica/complicaciones , Anemia Hemolítica/inmunología , Anemia Hemolítica Autoinmune/complicaciones , Anemia Hemolítica Autoinmune/inmunología , Artritis Reumatoide/complicaciones , Artritis Reumatoide/inmunología , Enfermedades Autoinmunes/etiología , Enfermedades Autoinmunes/inmunología , Linfocitos B/inmunología , Inmunodeficiencia Variable Común/diagnóstico , Inmunodeficiencia Variable Común/inmunología , Femenino , Humanos , Hipergammaglobulinemia/complicaciones , Hipergammaglobulinemia/inmunología , Inmunoglobulina M , Inmunoglobulinas Intravenosas/administración & dosificación , Inmunoglobulinas Intravenosas/uso terapéutico , Inmunofenotipificación , Lactante , Cirrosis Hepática Biliar/complicaciones , Cirrosis Hepática Biliar/inmunología , Trasplante de Hígado , Masculino , Persona de Mediana Edad , Estudios Multicéntricos como Asunto , Miastenia Gravis/complicaciones , Miastenia Gravis/inmunología , Púrpura Trombocitopénica Idiopática/complicaciones , Púrpura Trombocitopénica Idiopática/inmunología , Estudios Retrospectivos , Esplenectomía , Síndrome , Trombocitopenia/complicaciones , Trombocitopenia/inmunología
9.
J Virol ; 74(14): 6433-41, 2000 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-10864655

RESUMEN

Human T-cell lymphotropic virus type 1 (HTLV-1) is the causative agent of a chronic progressive myelopathy called tropical spastic paraparesis/HTLV-1-associated myelopathy (TSP/HAM). In this disease, lesions of the central nervous system (CNS) are associated with perivascular infiltration by lymphocytes. We and others have hypothesized that these T lymphocytes infiltrating the CNS may play a prominent role in TSP/HAM. Here, we show that transient contact of human or rat astrocytes with T lymphocytes chronically infected by HTLV-1 impairs some of the major functions of brain astrocytes. Uptake of extracellular glutamate by astrocytes was significantly decreased after transient contact with infected T cells, while the expression of the glial transporters GLAST and GLT-1 was decreased. In two-compartment cultures avoiding direct cell-to-cell contact, similar results were obtained, suggesting possible involvement of soluble factors, such as cytokines and the viral protein Tax-1. Recombinant Tax-1 and tumor necrosis factor alpha (TNF-alpha) decreased glutamate uptake by astrocytes. Tax-1 probably acts by inducing TNF-alpha, as the effect of Tax-1 was abolished by anti-TNF-alpha antibody. The expression of glutamate-catabolizing enzymes in astrocytes was increased for glutamine synthetase and decreased for glutamate dehydrogenase, the magnitudes of these effects being correlated with the level of Tax-1 transcripts. In conclusion, Tax-1 and cytokines produced by HTLV-1-infected T cells impair the ability of astrocytes to manage the steady-state level of glutamate, which in turn may affect neuronal and oligodendrocytic functions and survival.


Asunto(s)
Astrocitos/metabolismo , Moléculas de Adhesión Celular Neuronal/metabolismo , Ácido Glutámico/metabolismo , Virus Linfotrópico T Tipo 1 Humano/metabolismo , Glicoproteínas de Membrana/metabolismo , Linfocitos T/metabolismo , Factor de Necrosis Tumoral alfa/metabolismo , Transportadoras de Casetes de Unión a ATP/genética , Transportadoras de Casetes de Unión a ATP/metabolismo , Sistema de Transporte de Aminoácidos X-AG , Animales , Animales Recién Nacidos , Transporte Biológico , Línea Celular , Células Cultivadas , Contactina 2 , Feto , Humanos , ARN Mensajero/metabolismo , Ratas , Linfocitos T/virología
12.
Hum Gene Ther ; 8(1): 15-25, 1997 Jan 01.
Artículo en Inglés | MEDLINE | ID: mdl-8989991

RESUMEN

Ad CFTR, a replication-deficient adenovirus expressing the human cystic fibrosis transmembrane conductance regulator (CFTR), was administered by aerosolization in a single escalating dose to three pairs (cohorts) of cystic fibrosis (CF) patients. Buffer only was administered to the nose and lungs 9-14 days before nasal instillation of virus followed the day after by aerosolization of Ad CFTR to the lung. Nasal doses (defined in terms of viral plaque forming units, pfu) were 10(5), 10(7), and 4 x 10(8), whereas aerosolized doses were 10(7), 10(8), 5.4 x 10(8) for each cohort, respectively. No acute toxic effects were observed in the first 4 weeks after virus treatment. Shedding of infectious Ad CFTR was never detected, whereas detection of vector DNA sequences and CFTR expression demonstrated DNA transfer to the nose and airways of patients. No significant deviations in immunological and inflammatory parameters were observed in serum and in bronchoalveolar lavage (BAL). Importantly, for all patients, the serum anti-adenovirus antibody levels did not change significantly from baseline and no antibodies against adenovirus were found in BAL.


Asunto(s)
Adenoviridae/metabolismo , Aerosoles/uso terapéutico , Regulador de Conductancia de Transmembrana de Fibrosis Quística/metabolismo , Terapia Genética , Adolescente , Adulto , Southern Blotting , Lavado Broncoalveolar , Regulador de Conductancia de Transmembrana de Fibrosis Quística/análisis , Regulador de Conductancia de Transmembrana de Fibrosis Quística/genética , ADN/análisis , Femenino , Expresión Génica/genética , Vectores Genéticos/genética , Humanos , Inmunohistoquímica , Masculino , Mucosa Nasal/citología , Mucosa Nasal/metabolismo , Reacción en Cadena de la Polimerasa , ARN Mensajero/análisis
13.
J Neuroimmunol ; 65(1): 1-9, 1996 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-8642058

RESUMEN

We have previously shown that, in experimentally inoculated mice, canine distemper virus (CDV), a neurotropic virus, selectively infects certain brain structures (hypothalamus, hippocampus, monoaminergic nuclei, etc). Here we demonstrate that tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta and IL-6 transcripts are selectively expressed in these CDV-targeted structures, except in the dentate gyrus, where cytokines are induced without prior CDV replication. The time-course of TNF-alpha expression vs. viral replication in the hypothalamus was different from that in hippocampus. In addition, we show that a substantial number of neurons express TNF-alpha and IL-6. These findings provide new insights into the possible participation of cytokines in the neurological disorders triggered by CDV infection.


Asunto(s)
Citocinas/genética , Virus del Moquillo Canino/inmunología , Hipocampo/inmunología , Hipotálamo/inmunología , Infecciones por Morbillivirus/inmunología , Animales , Secuencia de Bases , Citocinas/inmunología , Virus del Moquillo Canino/genética , Femenino , Regulación de la Expresión Génica , Regulación Viral de la Expresión Génica/inmunología , Hipocampo/citología , Hipocampo/virología , Hipotálamo/citología , Hipotálamo/virología , Hibridación in Situ , Interleucina-1/genética , Interleucina-1/inmunología , Interleucina-6/genética , Interleucina-6/inmunología , Ratones , Datos de Secuencia Molecular , Neuronas/inmunología , Neuronas/virología , Reacción en Cadena de la Polimerasa , ARN Mensajero/análisis , Factores de Tiempo , Factor de Necrosis Tumoral alfa/genética , Factor de Necrosis Tumoral alfa/inmunología
14.
C R Seances Soc Biol Fil ; 190(1): 109-42, 1996.
Artículo en Francés | MEDLINE | ID: mdl-8881273

RESUMEN

At present it is conceivable to think that gene therapy represents a way to treat or even prevent the respiratory manifestations of cystic fibrosis. Consistent to such a concept, there is sufficient evidence that Ad-CFTR, a recombinant replication-deficient adenovirus expressing the human cystic fibrosis transmembrane conductance regulator cDNA, can vectorize the expression of a functional CFTR (cystic fibrosis transmembrane conductance regulator) to the nasal and airway epithelia. The clinical protocol was designed to assess the safety of single escalating doses of a replication defective adenovirus expressing the cystic fibrosis transmembrane conductance regulator gene (Ad-CFTR) when administered to the tracheobronchial portion of the airways and whether biological efficacy of CFTR delivery could be demonstrated. Six cystic fibrosis patients received nasal instillation and subsequent aerosol (Optineb, Air Liquide, Paris, France) administration of Ad-CFTR the following day. Doses (pfu) applied to the nose were 10(5) (patients SG and PB), 10(7) (patients FP and EP) and 4 x 10(8) (patients DS and FG), while aerosolised doses were 10(7) (patients SG and PB), 10(8) (patients FP and EP) and 5.4 x 10(8) (patients DS and FG), respectively. No acute toxic effects, no increase in the titer of anti-adenovirus antibodies and no spreading or shedding of Ad-CFTR were detected. In one patient Ad-CFTR DNA was found in the urine and blood two days after aerosolisation. Ad-CFTR DNA was detected in nasal and bronchial brush samples, in BAL, in saliva and tonsils 21, 8, 14 and 4 days post virus administration, respectively. Ad-CFTR mRNA (RT-PCR on bronchial cells) and CFTR protein (immunochemistry on nasal and bronchial cells) were detected up to 14 days following Ad-CFTR administration. These results show that the nebulisation of Ad-CFTR is a possible approach for treating the respiratory manifestation of cystic fibrosis.


Asunto(s)
Adenoviridae/genética , Regulador de Conductancia de Transmembrana de Fibrosis Quística/administración & dosificación , Regulador de Conductancia de Transmembrana de Fibrosis Quística/genética , Fibrosis Quística/terapia , ADN Recombinante/administración & dosificación , Técnicas de Transferencia de Gen , Vectores Genéticos/genética , Adolescente , Adulto , Aerosoles , Animales , Virus Defectuosos/genética , Tolerancia a Medicamentos , Terapia Genética/métodos , Humanos , Recombinación Genética , Efectividad Biológica Relativa , Sistema Respiratorio/virología
15.
J Neuropathol Exp Neurol ; 54(2): 165-74, 1995 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-7876886

RESUMEN

Primitive neuroectodermal tumors are thought to result from disturbed differentiation of neuroepithelial stem cells. These tumor cells retain the capacity to differentiate toward the neuron or glia phenotype under extrinsic stimuli. Previously, we have developed a model for the differentiation of a medulloblastoma cell line (Dev cells) induced by infection with the human retrovirus HTLV-I. This virus delivers signals which trigger the Dev cells to differentiate toward an astrocytic lineage. The aim of this study was to characterize the time course of viral infection, to identify the soluble factors released and to analyze their effects on Dev cells. The early phase of viral replication is followed by latent infection. Viral infection induces glial differentiation in a subpopulation of cells and results in the death of others. The inflammatory cytokines TNF alpha, IL1 alpha and IL6 were detected in medium conditioned by infected Dev cells. TNF alpha was cytotoxic and cytostatic for subpopulations of Dev cells. Furthermore, TNF alpha treatment reproduced the modulation of expression of the major histocompatibility complex antigens (MHC class I) observed in infected Dev cells. These observations support the view that HTLV-I infection, which triggers glial differentiation of medulloblastoma Dev cells, also causes the release of soluble factors capable of downregulating proliferation of dividing tumor cells and of modifying their recognition by cellular immune effectors.


Asunto(s)
Infecciones por HTLV-I/inmunología , Antígenos de Histocompatibilidad Clase I/biosíntesis , Meduloblastoma/inmunología , Factor de Necrosis Tumoral alfa/fisiología , Diferenciación Celular , Niño , Citocinas/fisiología , Citometría de Flujo , Técnica del Anticuerpo Fluorescente , Genoma Viral , Virus Linfotrópico T Tipo 1 Humano/aislamiento & purificación , Humanos , Masculino , Meduloblastoma/patología , Meduloblastoma/virología , Fenotipo , Pruebas de Precipitina , Factores de Tiempo , Células Tumorales Cultivadas , Factor de Necrosis Tumoral alfa/metabolismo
16.
Eur Cytokine Netw ; 2(1): 47-50, 1991.
Artículo en Inglés | MEDLINE | ID: mdl-1651783

RESUMEN

The monitoring of plasma soluble interleukin-2 receptor (S IL-2R) concentrations has been proposed in organ transplantation, especially to detect early manifestations of rejection. In organ transplantation, immune activation occurs in various circumstances such as rejections and infections. We performed S IL-2R determination 3 times a week in the sera of 106 patients undergoing kidney and/or pancreas transplantation. In kidney transplantation, S IL-2R was increased before the transplant. It also increased under prophylactic and especially under curative anti-rejection OKT3 or ATG therapy. In 90% cases, S IL-2R increased 2 to 4 days before creatininemia rise. In the other 10% cases, no correlation could be found with any clinical status modification. S IL-2R concentrations never increased in isolated acute tubular necrosis or in cyclosporine A (CsA) nephrotoxicity. In pancreas transplantation, the correlation between S IL-2R concentrations and possible pancreas rejection, was very poor. During cytomegalovirus (CMV) infection, only 50% patients with clinical CMV manifestations had high concentrations of S IL-2R. During Dihydroxy Propoxy Methyl Guanine (DPHG = Ganciclovir) treatment, S IL-2R still increased at the beginning, then it decreased progressively when therapy was efficient on CMV infection. The monitoring of S IL-2R concentrations may be useful in the weeks following organ transplantation provided that results are interpreted in the context of clinical and other laboratory findings, particularly with the renal function status and creatininemia.


Asunto(s)
Trasplante de Riñón/inmunología , Trasplante de Páncreas/inmunología , Receptores de Interleucina-2/sangre , Creatinina/sangre , Infecciones por Citomegalovirus/inmunología , Rechazo de Injerto/inmunología , Humanos , Solubilidad , Factores de Tiempo
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