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ÍtemSolo MetadatosPhosphodiesterase inhibitor pentoxifylline: An antiinflammatory/immunomodulatory drug potentially useful in some rheumatic diseases(1995-01-01) Anaya, Juan-Manuel; Espinoza, L.Phosphodiesterase inhibitor pentoxifylline: an antiinflammatory/immunomodulatory drug potentially useful in some rheumatic diseases: Adjuvants, Immunologic/therapeutic use, Animals, Anti-Inflammatory Agents, Non-Steroidal/therapeutic use, Arthritis, Rheumatoid/drug therapy in Humans- ÍtemSolo MetadatosThe putative protective role of hepatitis B virus (HBV) infection from autoimmune disorders(2008) Ram, Maya; Anaya, Juan-Manuel; Barzilai, Ori; Izhaky, David; Katz, Bat-sheva Porat; Blank, Miri; Shoenfeld, YehudaBackground: The etiology of autoimmune diseases is not fully clarified and the mechanisms underlying their initiation and progression are still obscure. It is becoming clear that in a genetic susceptible individual an environmental trigger such as infectious agent in general and viruses in particular could initiate the development of an autoimmune disease. Hepatitis B virus (HBV) is notorious in its association with diverse autoimmune diseases. Therefore, we aimed to determine the presence of hepatitis B core antibody (HBcAb), a seromarker for past or present infection with HBV, in a large number of sera collected from patients with different autoimmune diseases. Methods: A cohort of 675 sera samples of 5 different autoimmune diseases and healthy donors were screened for evidence of a prior infection with HBV. All samples were tested for hepatitis B core antibody (IgG) using the Monolisa anti-HBc PLUS commercial kit (Bio-Rad, Hercules, San Francisco, USA). Results: Lower percentage of HBcAb was found in sera of the autoimmune diseases when compared to normal controls. Fifteen (10.7%) from 140 normal controls were found positive for the presence of HBcAb. Two (2%) out of 98 multiple sclerosis (MS) sera were positive for the presence of HBcAb (OR: 0.17, 95%CI: 0.03-0.77, p = 0.01), 3 (2.5%) out of 117 systemic lupus erythematosus (SLE) sera (OR: 0.2, 95%CI: 0.06-0.77, p = 0.01), 4 (4.5%) out of 89 type 1 diabetes (T1D), 5 (6.1%) from 82 Sjogren's syndrome (SS) sera and 12 (8%) from 149 rheumatoid arthritis (RA) sera were positive for the presence of HBcAb. Conclusions: Our data divulge an unexpected low percentage of antibodies to HBcAg in patients with SLE, MS and T1D in comparison to healthy matched donors. This finding may raise a protective role to HBV in some autoimmune diseases i.e. hygiene theory. © 2008 Elsevier B.V. All rights reserved.
- ÍtemAcceso Abierto
Novel and rare functional genomic variants in multiple autoimmune syndrome and Sjögren's syndrome(2015) Johar, Angad S; Mastronardi, Claudio; Rojas-Villarraga, Adriana; Patel, Hardip R; Chuah, Aaron; Peng, Kaiman; Higgins, Angela; Milburn, Peter; Palmer, Stephanie; Silva‑Lara, Maria Fernanda; Velez, Jorge I; Andrews, Dan; Field, Matthew; Huttley, Gavin; Goodnow, Chris; Anaya, Juan-Manuel; Arcos-Burgos, MauricioBackground: Multiple autoimmune syndrome (MAS), an extreme phenotype of autoimmune disorders, is a very well suited trait to tackle genomic variants of these conditions. Whole exome sequencing (WES) is a widely used strategy for detection of protein coding and splicing variants associated with inherited diseases. Methods: The DNA of eight patients affected by MAS [all of whom presenting with Sjögren's syndrome (SS)], four patients affected by SS alone and 38 unaffected individuals, were subject to WES. Filters to identify novel and rare functional (pathogenic-deleterious) homozygous and/or compound heterozygous variants in these patients and controls were applied. Bioinformatics tools such as the Human gene connectome as well as pathway and network analysis were applied to test overrepresentation of genes harbouring these variants in critical pathways and networks involved in autoimmunity. Results: Eleven novel and rare functional variants were identified in cases but not in controls, harboured in: MACF1, KIAA0754, DUSP12, ICA1, CELA1, LRP1/STAT6, GRIN3B, ANKLE1, TMEM161A, and FKRP. These were subsequently subject to network analysis and their functional relatedness to genes already associated with autoimmunity was evaluated. Notably, the LRP1/STAT6 novel mutation was homozygous in one MAS affected patient and heterozygous in another. LRP1/STAT6 disclosed the strongest plausibility for autoimmunity. LRP1/STAT6 are involved in extracellular and intracellular anti-inflammatory pathways that play key roles in maintaining the homeostasis of the immune system. Further; networks, pathways, and interaction analyses showed that LRP1 is functionally related to the HLA-B and IL10 genes and it has a substantial impact within immunological pathways and/or reaction to bacterial and other foreign proteins (phagocytosis, regulation of phospholipase A2 activity, negative regulation of apoptosis and response to lipopolysaccharides). Further, ICA1 and STAT6 were also closely related to AIRE and IRF5, two very well known autoimmunity genes. Conclusions: Novel and rare exonic mutations that may account for autoimmunity were identified. Among those, the LRP1/STAT6 novel mutation has the strongest case for being categorised as potentially causative of MAS given the presence of intriguing patterns of functional interaction with other major genes shaping autoimmunity. © Johar et al. - ÍtemAcceso AbiertoPrimary immunodeficiency and autoimmunity: A comprehensive review(2019) Amaya-Uribe L.; Rojas M.; Azizi G.; Anaya, Juan-Manuel; Gershwin M.E.The primary immunodeficiency diseases (PIDs) include many genetic disorders that affect different components of the innate and adaptive responses. The number of distinct genetic PIDs has increased exponentially with improved methods of detection and advanced laboratory methodology. Patients with PIDs have an increased susceptibility to infectious diseases and non-infectious complications including allergies, malignancies and autoimmune diseases (ADs), the latter being the first manifestation of PIDs in several cases. There are two types of PIDS. Monogenic immunodeficiencies due to mutations in genes involved in immunological tolerance that increase the predisposition to develop autoimmunity including polyautoimmunity, and polygenic immunodeficiencies characterized by a heterogeneous clinical presentation that can be explained by a complex pathophysiology and which may have a multifactorial etiology. The high prevalence of ADs in PIDs demonstrates the intricate relationships between the mechanisms of these two conditions. Defects in central and peripheral tolerance, including mutations in AIRE and T regulatory cells respectively, are thought to be crucial in the development of ADs in these patients. In fact, pathology that leads to PID often also impacts the Treg/Th17 balance that may ease the appearance of a proinflammatory environment, increasing the odds for the development of autoimmunity. Furthermore, the influence of chronic and recurrent infections through molecular mimicry, bystander activation and super antigens activation are supposed to be pivotal for the development of autoimmunity. These multiple mechanisms are associated with diverse clinical subphenotypes that hinders an accurate diagnosis in clinical settings, and in some cases, may delay the selection of suitable pharmacological therapies. Herein, a comprehensively appraisal of the common mechanisms among these conditions, together with clinical pearls for treatment and diagnosis is presented. © 2019 Elsevier Ltd
- ÍtemAcceso AbiertoDepresión y familia en pacientes con artritis reumatoide(2002) Cadena, José; Cadavid, Martha; Ocampo, Maria Victoria; Vélez Ángel, María Clara; Anaya, Juan-ManuelObjetivos: Estudiar la prevalencia de depresión y las características de las relaciones familiares en pacientes con artritis reumatoide (AR). Métodos: Estudio transversal y descriptivo. La depresión fue evaluada mediante la escala de Zung. El estado de salud de los pacientes y las características familiares fueron evaluados por encuesta dirigida. Resultados: Se incluyeron 107 pacientes. Se observó una alta tasa de depresión (58%), y una baja proporción de satisfacción con el entorno laboral (40%) y con la situación del país (7%). La relación con el núcleo familiar fue considerada buena en la mayoría de los casos, con una proporción importante de satisfacción (60%). Dentro del núcleo familiar, quienes más colaboran con el paciente son la pareja (53%) y los hijos (63%), quienes, a través de una actitud de escucha, logran que el paciente con AR se sienta apoyado. Conclusión: La depresión es frecuente en los pacientes con AR, a pesar de tener un buen entorno familiar, el cual parece actuar ejerciendo un efecto amortiguador en el impacto de la enfermedad sobre la calidad de vida.
- ÍtemAcceso AbiertoSTAT4 but not TRAF1/C5 variants influence the risk of developing rheumatoid arthritis and systemic lupus erythematosus in Colombians(2008) Palomino-Morales, R J; Rojas-Villarraga, A; González, C I; Ramírez, G; Anaya, Juan-Manuel; Martín, JThe aim of this study was to determine the influence of STAT4 (rs7574865) and TRAF1/C5 (rs10818488 and rs2900180) gene polymorphisms on the risk of developing rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) in a Colombian population. This was a case-control study in which 839 individuals with RA (N = 274) and SLE (N = 144) and matched healthy controls (N = 421) were included. Genotyping was performed by using a polymerase chain reaction system with pre-developed TaqMan allelic discrimination assay. STAT4 rs7574865T allele disclosed a significant influence on the risk of developing SLE (P = 0.0005; OR 1.62, 95% CI 1.22-2.16) and RA (P = 0.008; OR 1.36; 95% CI 1.08-1.71), whereas no effect on these autoimmune diseases was observed for the TRAF1/C5 polymorphisms examined. Our data strengthen STAT4 rs7574865 polymorphism as a susceptibility factor for RA and SLE and provide further evidence for a common origin of autoimmune diseases.
- ÍtemSolo MetadatosAutoimmunity co-signaling system: Regulatory T cells, CTLA-4 and FOXP3(2005) Gómez Osorio L.M.; Martín Ibañez J.; Anaya, Juan-ManuelCo-signaling molecules can act as co-stimulators or co-inhibitors, depending on whether they promote or suppress T-cell activation, respectively. At the specific time and location, co-signaling molecules positively and negatively control antigen presentation, growth, differentiation and function of T-cells. An important cellular group implicated in the regulation of co-stimulation is known as regulatory T cells (Treg). These cells can be used clinically in treatments ranging from cellular transfer in transplant patients to autoimmune diseases and suppression in cancer patients. Treg act through CTLA-4 molecules, which have the ability to suppress the co-stimulation signals and to stop the T cell response. Recently, CTLA-4Ig fusion molecules have been developed, which can block the presentation of auto-antigens. FOXP3 transcription factor is a specific molecule present in Treg that inhibits the production of IL-2 by CD4+ activated cells. Currently, FOXP3 functions are being extensively studied in order to develop new therapeutic targets. This article reviews co-signaling and its mechanism in Treg (CTLA-4, FOXP3), as well as its role in the physiopathology of autoimmune diseases.
- ÍtemSolo MetadatosExpansion of gut associated immunoglobulin A secreting lymphocytes in rheumatoid arthritis correlates with high levels of serum IgA(1993) Anaya, Juan-Manuel; Sany, J.; Jorgensen, C.; Barneon, G.We report the emergence of polyclonal expansion of gut lymphocyte associated tissues producing IgA in a patient with rheumatoid arthritis associated with a high serum IgA concentration. The role of IgA in rheumatoid arthritis is reviewed.
- ÍtemAcceso AbiertoLatent Autoimmune Thyroid Disease(2020) Rodríguez Velandia, Yhojan Alexis; Rojas Quintana, Manuel Eduardo; Monsalve Carmona, Diana Marcela; Acosta Ampudia, Yeny Yasbleidy; Pacheco Nieva, Yovana; Rodríguez Jiménez, Mónica María del Pilar; Ramírez Santana, Heily Carolina; Anaya, Juan-ManuelObjetivo Determinar la prevalencia de autoanticuerpos tiroideos y los factores asociados en sujetos eutiroideos. Métodos Se incluyeron 300 sujetos eutiroideos, elegidos por muestreo estratificado de una cohorte inicial de 1335 individuos. La función tiroidea se evaluó midiendo los niveles séricos de TSH (0.3–4.5 ?IU / mL) y FT4 (5.2–12.7?g / dL). Los anticuerpos anti-peroxidasa (TPOAbs), anti-tiroglobulina (TgAbs) y anti-receptor de TSH (TrAbs) se evaluaron con 23 autoanticuerpos adicionales, así como con niveles de vitamina D (VitD). El análisis incluyó características sociodemográficas, clínicas y ambientales. Los datos se analizaron mediante pruebas bivariadas y multivariadas. Resultados Se observó autoinmunidad tiroidea en el 15,3% de los sujetos (TPOAbs 11,3% y TgAbs 2,0%). En seis individuos, ambos autoanticuerpos fueron positivos. Los TrAbs no se detectaron en ningún individuo. Enfermedad tiroidea familiar (? = 3.4, IC 95%: 1.2–9.5, P = 0.021), la presencia de otras enfermedades autoinmunes (? = 10.8, IC 95%: 1.6–72.9, P = 0.014) Insuficiencia de VitD ( P = 0.030), nunca fume (? = 6.9, IC 95%: 1.6–30.4, P = 0.010), beba más de 4 tazas de café (? = 3.8, IC 95%: 1.1–13.1, P = 0.036), y un mayor número de años expuestos al humo de leña ( P = 0.04) se asociaron con autoinmunidad tiroidea. En el caso de TPOAbs, enfermedad de tiroides familiar (CI ? = 4,9, 95%: 1,7 a 14,0, P = 0,003), nunca fume (? = 5,7, IC 95%: 1,4 a 21,0, P = 0.002), y beber más de 4 tazas de café (? = 3.6, IC 95%: 1.1–13.1, P = 0.047) se asociaron con su positividad. Además, la presencia de anti – SS – A / Ro52 (? = 36.7, IC 95%: 2.5–549.9, P = 0.009) y anticuerpos anti-Ku (? = 10.2, IC 95%: 1.1–100.7, P = 0.046) también se asoció con TPOAbs. La presencia de ascendencia africana (? = 10.5, IC 95%: 1.7–63.2, P = 0.01), anti – SS – A / Ro52 (? = 15.8, IC 95%: 1.2–198.6, P = 0,03), y los anticuerpos anti-CENP-B (? = 31,2, IC 95%: 1,8 a 565,9 P = 0,02) se asociaron con TgAbs. Conclusión La autoinmunidad tiroidea latente no es rara. Los factores ambientales, genéticos e inmunológicos, así como los ancestros, son factores de riesgo asociados. Estos resultados facilitarían la implementación de estrategias de detección para proporcionar un diagnóstico y tratamiento oportunos.
- ÍtemSolo MetadatosLa résilience chez les patientes atteintes de maladies auto-immunes(2019-05-01) Rojas M.; Rodriguez Y.; Pacheco Y.; Zapata E.; Monsalve Carmona, Diana Marcela; Mantilla R.D.; Rodríguez Jiménez, Mónica María del Pilar; Ramírez Santana, Heily Carolina; Molano González, Nicolás; Anaya, Juan-ManuelObjectif Évaluer le lien entre résilience et évolution clinique chez des patientes atteintes de maladies auto-immunes. Méthodes Les données de 188 femmes atteintes de maladies auto-immunes, incluant la polyarthrite rhumatoïde (n = 51), le lupus érythémateux systémique (n = 70), la sclérodermie systémique (n = 35) et le syndrome de Sjögren (n= 32), ont été collectées lors de groupes de discussion, d’entretiens individuels et de l’examen des dossiers médicaux. Les variables démographiques, cliniques et biologiques ont été analysées incluant l’activité de la maladie perçue par le patient. Pour mesurer la résilience, nous avons eu recours à la brève échelle de résilience. La régression linéaire multiple et bivariée et les arbres de classification et de régression ont été utilisés pour l’analyse des données.
