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1.
Rev. cuba. endocrinol ; 31(3): e203, sept.-dic. 2020. tab
Article in Spanish | LILACS, CUMED | ID: biblio-1156393

ABSTRACT

Introducción: Las bases fisiopatológicas del Síndrome de ovario poliquístico pueden predisponer a mayor riesgo de autoinmunidad a las mujeres que tienen esta condición y existen evidencias, aunque escasas, de mayor prevalencia de autoinmunidad tiroidea en ellas. Objetivos: Determinar la frecuencia de marcadores serológicos de autoinmunidad tiroidea en mujeres con Síndrome de ovario poliquístico e identificar si existe asociación entre la presencia de ellos y las concentraciones de progesterona y testosterona. Métodos: Se realizó un estudio en 50 mujeres con Síndrome de ovario poliquístico y 50 sin el síndrome. Se realizaron determinaciones de autoanticuerpos tiroideos (anti tiroglobulina (Anti-Tg) y anti peroxidasa (anti-TPO) a las mujeres de ambos grupos de estudio. Se realizaron determinaciones de hormonas (testosterona y progesterona) solo al grupo de estudio de mujeres con SOP. Se crearon categorías por anticuerpos: Positivo si los títulos fueron superior al rango de referencia y negativo dentro del rango. Se consideró respuesta autoinmune positiva, cuando al menos uno de los anticuerpos se encontró elevado. Para la asociación entre la presencia de autoinmunidad y las variables independientes se hicieron análisis bivariados mediante comparación de medias y test no paramétricos. Se consideró un nivel de significancia de α = 0,05. Resultados: En las mujeres con Síndrome de ovario poliquístico, 62 por ciento mostraron anticuerpos positivos y 14 por ciento en las sin el síndrome. En las mujeres sin síndrome, de las 7 mujeres con marcadores de autoinmunidad positivos, en 6 (85,7 por ciento) el anti-Tg fue el que dio positivo. No hubo diferencias significativas en cuanto a la asociación con los niveles de testosterona y progesterona. Conclusiones: Las mujeres con Síndrome de ovario poliquístico tienen mayor frecuencia de desarrollar respuesta autoinmune tiroidea, independiente de los niveles de progesterona y testosterona(AU)


Introduction: The physio-pathological bases of polycystic ovary syndrome may predispose women with this condition to a higher risk of autoimmunity and there is evidence, albeit scarce, of higher prevalence of thyroid autoimmunity in them. Objectives: Determine the frequency of serological markers of thyroid autoimmunity in women with polycystic ovary syndrome and identify whether there is an association between the presence of them and progesterone and testosterone concentrations. Methods: A study was conducted in 50 women with polycystic ovary syndrome and 50 without the syndrome. Determinations of thyroid autoantiantibodies (anti-thyroglobulin (Anti-Tg) and anti-peroxidase (anti-TPO) were made to women in both study groups. Hormone determinations (testosterone and progesterone) were made only to the study group of women with PCOS. Categories were created by antibodies: Positive if the titles were greater than the reference range, and negative if within the range. It was considered a positive autoimmune response when at least one of the antibodies was found increased. For the association between the presence of autoimmunity and independent variables, bivariate analyses were performed by means comparison and non-parametric tests. It was considered a significance level of α =0.05. Results: In women with polycystic ovary syndrome, 62 percent showed positive antibodies and 14 percent in those without the syndrome. In women without the syndrome, of the 7 women with positive autoimmune markers, in 6 (85.7 percent) the anti-Tg was the one that tested positive. There were no significant differences in the association with testosterone and progesterone levels. Conclusions: Women with polycystic ovary syndrome are more often able to develop thyroid autoimmune response, independently from the progesterone and testosterone levels(AU)


Subject(s)
Humans , Polycystic Ovary Syndrome/epidemiology , Thyroid Gland/physiopathology , Autoimmunity/physiology , Hormones/analysis , Antibodies , Testosterone/analysis , Thyroglobulin/administration & dosage , Case-Control Studies
2.
An. bras. dermatol ; 94(2): 133-146, Mar.-Apr. 2019. tab, graf
Article in English | LILACS | ID: biblio-1001150

ABSTRACT

Abstract: Bullous pemphigoid is the most frequent autoimmune bullous disease and mainly affects elderly individuals. Increase in incidence rates in the past decades has been attributed to population aging, drug-induced cases and improvement in the diagnosis of the nonbullous presentations of the disease. A dysregulated T cell immune response and synthesis of IgG and IgE autoantibodies against hemidesmosomal proteins (BP180 and BP230) lead to neutrophil chemotaxis and degradation of the basement membrane zone. Bullous pemphigoid classically manifests with tense blisters over urticarial plaques on the trunk and extremities accompanied by intense pruritus. Mucosal involvement is rarely reported. Diagnosis relies on (1) the histopathological evaluation demonstrating eosinophilic spongiosis or a subepidermal detachment with eosinophils; (2) the detection of IgG and/or C3 deposition at the basement membrane zone using direct or indirect immunofluorescence assays; and (3) quantification of circulating autoantibodies against BP180 and/or BP230 using ELISA. Bullous pemphigoid is often associated with multiple comorbidities in elderly individuals, especially neurological disorders and increased thrombotic risk, reaching a 1-year mortality rate of 23%. Treatment has to be tailored according to the patient's clinical conditions and disease severity. High potency topical steroids and systemic steroids are the current mainstay of therapy. Recent randomized controlled studies have demonstrated the benefit and safety of adjuvant treatment with doxycycline, dapsone and immunosuppressants aiming a reduction in the cumulative steroid dose and mortality.


Subject(s)
Humans , Aged , Pemphigoid, Bullous/diagnosis , Steroids/therapeutic use , Autoimmunity/physiology , Fluorescent Antibody Technique/methods , Pemphigoid, Bullous/classification , Pemphigoid, Bullous/etiology , Pemphigoid, Bullous/drug therapy , Diagnosis, Differential
3.
Rev. Assoc. Med. Bras. (1992) ; 63(12): 1090-1099, Dec. 2017. graf
Article in English | LILACS | ID: biblio-896334

ABSTRACT

Summary Previous studies have demonstrated the expression of the CD25 marker on the surface of naturally occurring T cells (Tregs) of mice, which have a self-reactive cellular profile. Recently, expression of other markers that aid in the identification of these cells has been detected in lymphocyte subtypes of individuals suffering of autoimmune and idiopathic diseases, including: CD25, CTLA-4 (cytotoxic T-lymphocyte antigen 4), HLA-DR (human leukocyte antigen) and Interleukin 10 (IL-10), opening new perspectives for a better understanding of an association between such receptors present on the cell surface and the prognosis of autoimmune diseases. The role of these molecules has already been described in the literature for the modulation of the inflammatory response in infectious and parasitic diseases. Thus, the function, phenotype and frequency of expression of the a-chain receptor of IL-2 (CD25) and IL-10 in lymphocyte subtypes were investigated. Murine models have been used to demonstrate a possible correlation between the expression of the CD25 marker (on the surface of CD4 lymphocytes) and the control of self-tolerance mechanisms. These studies provided support for the presentation of a review of the role of cells expressing IL-2, IL-10, HLA-DR and CTLA-4 receptors in the monitoring of immunosuppression in diseases classified as autoimmune, providing perspectives for understanding peripheral regulation mechanisms and the pathophysiology of these diseases in humans. In addition, a therapeutic approach based on the manipulation of the phenotype of these cells and ways of scintigraphically monitoring the manifestations of these diseases by labeling their receptors is discussed as a perspective. In this paper, we have included the description of experiments in ex vivo regulation of IL-10 and synthesis of thio-sugars and poly-sugars to produce radiopharmaceuticals for monitoring inflammation. These experiments may yield benefits for the treatment and prognosis of autoimmune diseases.


Resumo Estudos anteriores já haviam demonstrado a expressão do marcador CD25 na superfície de células T de ocorrência natural (Tregs) de camundongos, que apresentam perfil celular autorreativo. Recentemente, foi detectada, em subtipos de linfócitos de indivíduos acometidos por doenças autoimunes e de causa idiopática, a expressão de outros marcadores, que auxiliam na identificação dessas células, entre os quais: CD25, CTLA-4 (cytotoxic T-lymphocyte antigen 4), HLA-DR (human leucocyte antigen) e Interleucina 10 (IL-10), abrindo novas perspectivas para a melhor compreensão de uma associação entre esses receptores presentes na superfície celular e o prognóstico de doenças autoimunes. O papel dessas moléculas já havia sido descrito na literatura na modulação da resposta inflamatória em doenças infectoparasitárias. Dessa forma, foram investigados a função, o fenótipo e a frequência de expressão, do receptor de cadeia a da IL-2 (CD25) e de IL-10 em subtipos de linfócitos. O modelo murino tem sido utilizado para demonstrar uma possível correlação entre a expressão do marcador CD25 (na superfície de linfócitos CD4) e o controle dos mecanismos de autotolerância. Essas pesquisas forneceram suporte para apresentação de uma revisão sobre o papel das células que expressam os receptores de IL-2, IL-10, HLA-DR e CTLA-4 no monitoramento da imunossupressão, em doenças de classificação autoimune, abrindo perspectivas para o entendimento dos mecanismos de regulação periférica e sobre a fisiopatologia dessas doenças no ser humano. Além disso, é discutida como perspectiva uma abordagem terapêutica fundamentada na manipulação do fenótipo dessas células, bem como de modos de monitoramento cintilográfico das manifestações dessas doenças, por meio da marcação de seus receptores. Nestes, foram incluídas descrições das experiências em regulação ex-vivo de IL-10; de síntese de tioaçúcares e de poliaçúcares para produção de radiofármacos para monitoramento de inflamações. Essas experiências podem trazer benefícios na terapia e no prognóstico de doenças autoimunes.


Subject(s)
Humans , Animals , Autoimmune Diseases/diagnostic imaging , Autoimmunity/physiology , Interleukin-10/physiology , T-Lymphocytes, Regulatory/physiology , Prognosis , Autoimmune Diseases/immunology , Autoimmune Diseases/therapy , HLA-DR Antigens , Radionuclide Imaging , CD4 Antigens/immunology , Interleukin-10/immunology , Models, Animal , Interleukin-2 Receptor alpha Subunit/immunology , CTLA-4 Antigen , Immune Tolerance , Mice
4.
Rev. Fundac. Juan Jose Carraro ; 22(42): 46-49, 2017.
Article in Spanish | LILACS | ID: biblio-908171

ABSTRACT

Porphyromonas gingivalis (P.Gingivalis) es un microorganismo comprometido en el inicio y progresión de la enfermedad periodontal crónica y agresiva, y es considerado su principal agente etiológico. Esta bacteria cuenta con una serie de factores de virulencia que le permiten, iniciar el proceso infeccioso, perpetuar la infección y también transformar la placa dental benigna en una comunidad microbiana patógena. Estudiar sus factores de virulencia y su capacidad de modular la respuesta inmunológica del huésped es muy importante para comprender el papel de este patógeno en el desarrollo y establecimiento de la enfermedad. Esta revisión proporciona una visiónactual sobre los factores de virulencia y su impacto sobre la respuesta inmunológica en relación con la patogénesis de la enfermedad periodontal.


Subject(s)
Male , Female , Humans , Periodontal Diseases/microbiology , Porphyromonas gingivalis/pathogenicity , Virulence Factors , Autoimmunity/physiology , Immunity, Mucosal , Periodontal Diseases/etiology , Periodontal Diseases/pathology
5.
Rev. Círc. Argent. Odontol ; 73(222): 7-11, jun. 2016. ilus
Article in Spanish | LILACS | ID: lil-794298

ABSTRACT

El síndrome de Down es un factor de riesgo no modificable para la enfermedad periodontal; los individuos con síndrome de Down tienen una mayor prevalencia y severidad de enfermedad periodontal que no puede ser explicada únicamente por una higiene bucal deficiente, y diversos estudios sugieren que esto se debe a cambios en su respuesta inmune y en la composición microbiológica de su biofilm. En este trabajo se hará una revisión de las siguiente anormalidades del sistema inmune que fueron encontradas: - defectos en la quimiotaxis de los neutrófilos - fagocitosis parcial de los leucocitos contra los estafilococos - distribución alterada de subclases de IgG en saliva - aumentados niveles de prostaglandinas E2 - aumentada cantidad de metaloproteinasas de la matriz en el fluido gingival crevicular - reducida expresión de IL-10. Por estos motivos, la atención periodontal de los pacientes son síndrome de Down es ligeramente diferente...


Subject(s)
Humans , Dental Care for Chronically Ill/methods , Periodontal Diseases/etiology , Dental Plaque/microbiology , Down Syndrome/complications , Autoimmunity/physiology , Mouth Diseases/etiology , Periodontal Diseases/immunology , Tooth Diseases/etiology , Dental Plaque/therapy , Dental Scaling/methods
6.
Arq. neuropsiquiatr ; 74(1): 5-9, Jan. 2016. graf
Article in English | LILACS | ID: lil-772601

ABSTRACT

The mechanisms involved in the symptoms of Sydenham’s chorea (SC) remain obscure. Taking into account the autoreactive antibody-mediated hypothesis of SC pathogenesis, the persistence of chorea may be associated with increased levels of B1 lymphocytes and other lymphocyte subsets. We evaluated lymphocyte subsets, including B1 and T cells, in patients with remitted (RSC) and persistent (PSC) SC by flow cytometry. Our results showed neither difference in the frequency of T and B lymphocytes subpopulations nor in their activation and functional states. These findings undermine the view of PSC as a sustained cytotoxic cellular-mediated condition. Alternative mechanisms may explain the pathogenesis of PSC.


Os mecanismos subjacentes aos sintomas da coreia de Sydenham (CS) permanecem desconhecidos. Considerando-se a hipótese de que a patogênese da CS é mediada por anticorpos autorreativos, a persistência da coreia está provavelmente associada a níveis aumentados de linfócitos B1 e outros subtipos de linfócitos. No presente trabalho, foram avaliados subtipos de linfócitos B e T em pacientes com CS em remissão (CSR) e persistente (CSP), por citometria de fluxo. Nossos resultados demonstraram que não há diferença na frequência das subpopulações de linfócitos T e B circulantes e no perfil de ativação e estado funcional dessas células. Esses resultados enfraquecem a hipótese de que a CSP seja uma condição imune sustentada mediada por células citotóxicas. São necessários estudos que investiguem mecanismos alternativos que expliquem a patogênese da CSP.


Subject(s)
Adolescent , Adult , Female , Humans , Male , Young Adult , Autoimmunity/physiology , B-Lymphocyte Subsets/pathology , Chorea/immunology , T-Lymphocyte Subsets/pathology , B-Lymphocyte Subsets/immunology , Flow Cytometry , Lymphocyte Count , T-Lymphocyte Subsets/immunology
7.
Rev. Asoc. Odontol. Argent ; 102(2): 87-94, abr.-jun. 2014. tab
Article in Spanish | LILACS | ID: lil-724483

ABSTRACT

En la enfermedad periodontal, la acumulación de bacterias gramnegativas, genera una respuesta inmunoinflamatoria que es modulada por el mecanismo de defensa del paciente. El tratamiento de modulación del huésped (TMH), ha sido incorporado como una opción farmacológica para el control de la enfermedad periodontal. El objetivo de la revisión fue investigar los efectos de los inhibidores de la colagenasa tisular y de los analgésicos antiinflamatorios no esteroides (AINES) como agentes moduladores de la enfermedad periodontal. A tal fin, se realizó una búsqueda de estudios de casos, controles y revisiones, empleando las bases de datos Medline-PubMed, LILACS y Dialnet. Se encontró que los resultados de las terapias de modulación del huésped tienen como blanco los mediadores proinflamatorios y enzimas destructivas que degradan el colágeno y destruyen tejido óseo, equilibrando y aumentando las acciones antiinflamatorias y protectivas. Los fármacos usados en el TMH regulan los procesos destructivos de la respuesta inmunoinflamatoria en presencia de placa dental, sobre todo en pacientes susceptibles.


Subject(s)
Humans , Anti-Inflammatory Agents, Non-Steroidal/immunology , Autoimmunity/physiology , Periodontal Diseases/immunology , Periodontal Diseases/drug therapy , Case-Control Studies , Collagenases/physiology , Databases, Bibliographic
8.
Arq. bras. endocrinol. metab ; 58(1): 48-52, 02/2014. tab
Article in English | LILACS | ID: lil-705245

ABSTRACT

Objective : To establish whether there is a relationship between hyperprolactinemia and primary thyroid disorders, focusing on patients with autoimmune features. Materials and methods : The medical records of 100 patients with hyperprolactinemia (HPRL) were retrospectively examined. Records of thyroid ultrasonography (USG), basal serum levels of thyroid stimulating hormone, circulating free thyroxine, free triiodothyronine, antithyroglobulin (anti-Tg), and antithyroperoxidase (anti-TPO) antibodies were analyzed. In 100 control subjects, matched by age and gender with HPRL patients, thyroid USG, thyroid function tests (TFTs), and autoantibody panel were obtained. Results : The median PRL in patients was 93 ng/mL (range: 37-470). Twenty-five patients (25%) and 22 controls (22%) had positive anti-Tg and/or anti-TPO titers (P = 0.739). The median serum PRL was 98 (37-470) ng/mL in patients with positive thyroid autoantibodies, and 92 (40-470) ng/mL in patients who were negative (P = 0.975). Among the individuals with autoantibody positivity TFTs abnormalities were more frequent in HPRL patients (60%, out of 25 patients, 14 with subclinical hypothyroidism and one with hyperthyroidism) than in controls (9.1%, out of 22 patients, 2 with subclinical hyperthyroidism) (P < 0.001). Twenty-seven patients with HPRL and 31 controls had goiter (27 vs. 31%, P = 0.437). Forty-six patients (46%) and 50 (50%) controls had one or more of the features of thyroid disorder, which were goiter, positive thyroid autoantibody, and thyroid function abnormality (P = 0.888). Conclusion : HPRL may be associated with more severe thyroid dysfunction in patients with thyroid autoimmunity. .


Objetivo : Verificar se existe uma relação entre a hiperprolactinemia e distúrbios primários da tireoide, focando em pacientes com características autoimunes. Materiais e métodos : Os prontuários de 100 pacientes com hiperprolactinemia (HPRL) foram examinados retrospectivamente. Foram analisados registros de ultrassonografia da tireoide (USG), níveis séricos basais de hormônio tireoestimulante, tiroxina livre, triiodotironina livre e anticorpos antitireoglobulina (anti-Tg) e antitireoperoxidase (anti-TPO). Foram obtidos de 100 controles, pareados por idade e sexo com pacientes com HPRL, USG, testes de função da tireoide (TFTs) e painel de autoanticorpos. Resultados : A média de PRL em pacientes foi de 93 ng/mL (variação: 37-470). Vinte e cinco pacientes (25%) e 22 controles (22%) foram positivos para títulos de anti-Tg e/ou anti-TPO (P = 0,739). A mediana de PRL sérica foi de 98 (37-470) ng/mL em pacientes positivos para autoanticorpos tiroidianos e 92 (40-470) ng/mL em pacientes negativos (P = 0,975). Entre os indivíduos positivos para autoanticorpos, as anormalidades da TFTs foram mais frequentes em pacientes HPRL (60%; de 25 pacientes, 14 com hipotireoidismo subclínico e um com hipertireoidismo) do que nos controles (9,1%; de 22 pacientes, 2 com hipertireoidismo subclínico) (P < 0,001). Vinte e sete pacientes com HPRL e 31 controles apresentavam bócio (27 contra 31%; P = 0,437). Quarenta e seis pacientes (46%) e 50 (50%) controles tiveram uma ou mais das características de problemas de tireoide, como bócio, autoanticorpos antitireoide e anormalidades da função tiroidiana (P = 0,888). Conclusão : A HPRL pode estar associada à disfunção da tireoide mais grave em pacientes com autoimunidade contra a tireoide. .


Subject(s)
Adolescent , Adult , Aged , Female , Humans , Male , Middle Aged , Young Adult , Autoimmunity/physiology , Hyperprolactinemia/immunology , Prolactin/blood , Thyroid Gland/immunology , Autoantibodies/blood , Autoantigens/blood , Case-Control Studies , Goiter/diagnosis , Iodide Peroxidase/immunology , Retrospective Studies , Severity of Illness Index , Statistics, Nonparametric , Thyroid Function Tests , Thyroid Gland , Thyroiditis, Autoimmune/diagnosis , Thyrotropin/blood , Thyroxine/blood
9.
Rev. cuba. pediatr ; 85(2): 230-241, abr.-jun. 2013.
Article in Spanish | LILACS | ID: lil-678135

ABSTRACT

En la actualidad existen diversos productos farmacéuticos constituidos por inmunoglobulinas (fundamentalmente IgG), purificadas por diversos métodos, lo que implica que pueden ser administradas por diversas vías (intramuscular, intravenosa y subcutánea). Estos productos tienen un amplio espectro de indicaciones en diversas enfermedades. Las inmunoglobulinas son los efectores finales de la respuesta inmune humoral, por lo que sus indicaciones fundamentales incluyen la terapia de reemplazo en enfermedades que cursan con déficit en la producción de anticuerpos, las situaciones en que se necesita de manera inmediata la presencia de anticuerpos neutralizantes, como en las terapias posexposición, y en enfermedades que cursan con disrregulación de la respuesta inmune


There are presently several pharmaceuticals made up of immunoglobulines (fundamentally IgG) purified by several methods, which means that they can be administered by different routes (intramuscularly, intravenously and subcutaneously). These products have a wide spectrum of prescriptions for several diseases. The immunoglobulins are the final effectors of the humoral immune response, so their fundamental prescriptions cover replacement therapies in diseases with antibody production deficit, situations requiring immediate presence of neutralizing antibodies such as post-exposure therapies, and diseases with immune response deregulation


Subject(s)
Humans , Autoimmunity/physiology , Immunization, Passive/methods , Immunoglobulin G/therapeutic use , Pediatrics/ethics , Biological Therapy/methods
10.
Rev. cuba. invest. bioméd ; 30(4): 501-510, sep.-dic. 2011.
Article in Spanish | LILACS | ID: lil-615419

ABSTRACT

La autoinmunidad se caracteriza por una pérdida de la tolerancia inmunológica que produce la destrucción de células y tejidos propios. El sistema del complejo mayor de histocompatibilidad posee una fuerte asociación con las enfermedades autoinmunes aunque determinados genes que codifican para citoquinas y moléculas coestimuladoras incrementan la susceptibilidad genética. Estudios de concordancia entre gemelos monocigóticos demuestran el papel de los factores ambientales en la aparición de las enfermedades autoinmunes. A pesar de los avances científicos producidos en esta área de investigación, los mecanismos subyacentes de estas afecciones son desconocidos. El objetivo de este trabajo es exponer de forma sintetizada el papel de los factores genéticos, inmunológicos y ambientales en la autoinmunidad


The autoimmunity is characterized by a loss of immunologic tolerance producing the destruction of cells and own tissues. The major complex system of histocompatibility has a close association with the autoimmune diseases although determined genes codifying for cytokines and co-stimulators molecules increase the genetic susceptibility. Concordance studies among monozygotic twins demonstrate the role of environmental factors in appearance of autoimmune diseases. Despite the scientific advances achieved in this research field, the underlying mechanisms of these affections are unknown. The objective of present paper is to expose in a summarized way the role of the genetic, immunologic and environmental factors in autoimmunity


Subject(s)
Autoimmunity/physiology , Immunologic Factors/deficiency , Gene-Environment Interaction , Genetic Predisposition to Disease
11.
Arq. bras. endocrinol. metab ; 52(2): 315-321, mar. 2008. tab
Article in Portuguese | LILACS | ID: lil-481001

ABSTRACT

A prevalência do diabetes auto-imune latente do adulto (LADA) varia em virtude da população estudada, dos critérios usados e dos anticorpos avaliados. Em 256 pacientes com menos de 25 anos, encontramos 26 (10,2 por cento) com anticorpos anti-GAD (GADA) positivos, dos quais 16 (6,3 por cento) evoluíram sem necessidade de insulina inicialmente. Embora exista controvérsias, sugere-se como critérios diagnósticos de LADA: idade entre 25 e 65 anos; ausência de cetoacidose ou hiperglicemia sintomática no diagnóstico ou imediatamente após, sem necessidade de insulina por 6 a 12 meses; e presença de auto-anticorpos (especialmente GADA). A auto-imunidade e a resistência insulínica coexistem no LADA, e a contribuição desses fatores parece estar refletida nos títulos de GADA. Um subgrupo similar aos diabéticos tipo 2, fenotipicamente e na progressão para necessidade de insulina, parece ser melhor identificado pela presença de baixos títulos de GADA, sobretudo isolados. Por outro lado, indivíduos com altos títulos de GADA e múltiplos anticorpos apresentam fenótipo mais próximo do diabetes melito do tipo 1 (DM1) clássico e são de maior risco para falência prematura das células-beta. Comparados aos diabéticos GADA-negativos, pacientes com LADA apresentam maior prevalência de outros auto-anticorpos (anti-TPO, anti-21-hidroxilase e associados à doença celíaca) e maior freqüência de genótipos e haplótipos de risco para DM1. Pacientes com altos títulos de GADA podem ser beneficiados, retardando a falência das células-beta, com a insulinização precoce e evitando-se o uso de sulfoniluréias. Em oposição, pacientes com baixos títulos de GADA aparentemente não teriam prejuízos em serem conduzidos da mesma forma que pacientes portadores de diabetes melito tipo 2 (DM2) (GADA-negativos).


The prevalence of latent autoimmune diabetes of the adult (LADA) varies according to the population studied, criteria used and antibodies analyzed. In a series of 256 patients > 25 years, we found that 26 (10.2 percent) were anti-GAD antibody (GADA) positive and 16 of them (6.3 percent) progressed without initial insulin requirement. Although controversy exists, the following diagnostic criteria for LADA are suggested: age between 25 and 65 years; absence of ketoacidosis or symptomatic hyperglycemia at diagnosis or immediately thereafter, without insulin requirement for 6-12 months; and presence of autoantibodies (especially GADA). Autoimmunity and insulin resistance coexist in LADA and the contribution of these factors seems to be reflected in GADA titers. A subgroup, which is phenotypically and in terms of insulin requirement similar to type 2 diabetic patients, seems to be better identified based on the presence of low GADA titers, especially when these antibodies are present alone. On the other hand, subjects with high GADA titers and multiple antibodies show a phenotype close to that of classical DM 1 and are at a higher risk of premature beta-cell failure. Compared to GADA-negative diabetics, patients with LADA present a higher prevalence of other autoantibodies (anti-TPO, anti-21-hydroxylase and antibodies associated with celiac disease) and a higher frequency of genotypes and haplotypes indicating a risk for DM 1. Patients with high GADA titers may benefit from early insulinization and avoiding the use of sulfonylureas, delaying beta-cell failure. In contrast, patients with low GADA titers do not seem to have any disadvantage when managed as type 2 diabetic patients (GADA negative).


Subject(s)
Adult , Aged , Aged, 80 and over , Humans , Middle Aged , Young Adult , Diabetes Mellitus, Type 1 , Autoantibodies/analysis , Autoimmunity/physiology , Biomarkers/analysis , Brazil/epidemiology , C-Peptide/analysis , Diagnosis, Differential , Diabetes Mellitus, Type 1/diagnosis , Diabetes Mellitus, Type 1/drug therapy , Diabetes Mellitus, Type 1/epidemiology , Diabetes Mellitus, Type 1/immunology , /diagnosis , /drug therapy , /epidemiology , /immunology , Genetic Predisposition to Disease , Glutamate Decarboxylase/analysis , Glutamate Decarboxylase/immunology , Hypoglycemic Agents/therapeutic use , Insulin Resistance/physiology , Insulin/therapeutic use , Prevalence , Young Adult
13.
Rev. méd. Chile ; 134(9): 1175-1184, sept. 2006. ilus, tab
Article in Spanish, English | LILACS | ID: lil-438422

ABSTRACT

BAFF (B cell activating factor belonging to the TNF family) is a cytokine implicated in the survival and maturation of peripheral B lymphocytes and T and B cell activation. BAFF binds to three different receptors: TACI, BCMA and BAFF-R, whose expression is restricted to B and T lymphocytes. BAFF and BAFF-R-deficient mice show a dramatic loss of peripheral B lymphocytes and a severely reduced immune response. In contrast, an enhanced BAFF expression leads to B cell hyperplasia and autoimmunity in mice. In vivo, administration of soluble decoy receptors for BAFF effectively decreases disease progression in various autoimmune mouse models. These evidences render BAFF as a potentially new therapeutic target. Elevated BAFF levels have been detected in the serum of patients with autoimmune diseases, such as Systemic Lupus Erythematosus, rheumatoid arthitis, Sjõgren's syndrome, lymphoid cancers and HIV infection. In addition to BAFF receptors, malignant B cells abnormally express BAFF, which attenuates apoptosis through both autocrine and paracrine pathways. The data suggest that an increase in the expression of BAFF induces an enhanced B and T cell activation and the survival of pathologically active B cells. In this article, we review and discuss the participation of BAFF and its receptors in the immune response and its involvement in immunodeficiency, autoimmunity, infections and lymphoid cancers as well as the currently investigated therapies using BAFF antagonists in the treatment of these diseases.


Subject(s)
Animals , Humans , Autoimmune Diseases/immunology , Autoimmunity/physiology , B-Cell Activating Factor/immunology , B-Lymphocytes/immunology , Cytokines/immunology , Lymphoma/immunology , Autoimmune Diseases/metabolism , B-Cell Activating Factor/metabolism , B-Lymphocytes/metabolism , Cytokines/metabolism , Disease Models, Animal , Lymphoma/metabolism , Receptors, Tumor Necrosis Factor/immunology , Receptors, Tumor Necrosis Factor/metabolism
14.
Rev. invest. clín ; 57(3): 447-456, may.-jun. 2005. ilus, tab
Article in Spanish | LILACS | ID: lil-632466

ABSTRACT

Prolactin (PRL) Is a 23 κDa protein hormone that is produced and secreted by the pituitary lactotrophs. Although PRL was initially regarded as an exclusive pituitary hormone, many nonpituitary tissues were later found to contain and produce this hormone. The most established extrapituitary sites that produce PRL are the decidua, the immune system, brain and endometrium. In the immune system, PRL acts as a cytokine where it plays an important role in human immune responses, including in autoimmune diseases. Here, we will discuss the regulation of PRL gene expression in human lymphocytes and review the functions of PRL made by the immune cells, including its involvement in autoimmunity.


La prolactina es una hormona que fue considerada durante mucho tiempo de origen exclusivamente hipofisario, y cuya función más importante era la promoción de la lactancia. Sin embargo, la prolactina no sólo se sintetiza en diversos sitios del organismo, sino que también participa en una amplia variedad de procesos biológicos. Dentro de los sitios de síntesis extrahipofisarios de esta hormona se encuentran diversas células del sistema inmunológico. A este nivel, la prolactina actúa afectando desde la proliferación celular hasta el estado inmune del individuo. En esta revisión presentamos algunos aspectos relativos a la prolactina de origen linfocitario tales como su síntesis, su participación en el sistema inmunológico y su relación con estados de autoinmunidad.


Subject(s)
Animals , Female , Humans , Male , Mice , Immune System/physiology , Prolactin/physiology , Autocrine Communication , Autoimmune Diseases/metabolism , Autoimmunity/physiology , Cell Differentiation/physiology , Disease Models, Animal , Gene Expression Regulation , Leukocytes/metabolism , Lupus Erythematosus, Systemic/metabolism , Lymphocytes/metabolism , Mice, Inbred NZB , Paracrine Communication , Pituitary Gland, Anterior/metabolism , Pituitary Gland, Anterior , Prolactin/genetics , Promoter Regions, Genetic/genetics , Receptors, Cytokine/physiology , Receptors, Prolactin/metabolism , Transcription, Genetic
17.
Perinatol. reprod. hum ; 14(2): 88-97, abr.-jun. 2000. tab
Article in Spanish | LILACS | ID: lil-286333

ABSTRACT

La capacidad de respuesta del sistema inmune (SI), no es la misma a lo largo de la vida, se ha observado que las infecciones son más frecuentes durante el primer año de vida que en la vida adulta, lo cual parece indicar que los neonatos son incapaces de desarrollar una respuesta inmunológica eficaz, durante la etapa de los retos inmunológicos primarios. Se han descrito diferencias fenotípicas y funcionales entre el SI del neonato y del adulto; con base en ellas se piensa que el SI del neonato es "inmaduro". Sin embargo, también se han realizado acercamientos experimentales que demuestran una capacidad similar de la respuesta celular, en neonatos y adultos. De estos ensayos se concluye que la inmadurez observada en el neonato, no es inicialmente debida a defectos cualitativos (por la capacidad de respuesta de las células); sino a las condiciones en las que se realiza el estímulo inmunológico. El presente artículo pretende proporcionar información actualizada sobre la naturaleza y desarrollo de la respuesta inmunológica en el neonato.


Subject(s)
Immune System/physiology , Receptors, Cytokine/immunology , Infant, Newborn/immunology , Autoimmunity/physiology , Phenotype , T-Lymphocytes/immunology
19.
In. Palomo González, Iván; Ferreira Vigoroux, Arturo; Sepúlveda Carvajal, Cecilia; Rosemblatt Silber, Mario; Vergara Castillo, Ulises. Fundamentos de inmunología. Talca, Universidad de Talca, 1998. p.305-15, ilus.
Monography in Spanish | LILACS | ID: lil-284813
20.
Rev. bras. alergia imunopatol ; 20(6): 223-7, nov.-dez. 1997. ilus
Article in Portuguese | LILACS | ID: lil-209704

ABSTRACT

Existe atualmente grande discussao a respeito do valor da Imunoterapia nas doenças alérgicas. Porém, à luz de novos conhecimentos sobre o sistema imune e particularmente as populaçoes de linfócitos TH1 e TH2 e do tipo predominante de resposta que provocam, é necessário reavaliaçao desta imunoterapia e especialmente da sua precocidade para os dois três primeiros anos de vida. Discutem-se o valor da regulaçao das populaçoes TH1 e TH2, os fatores que influenciam esta regulaçao, o papel dos vírus respiratórios, a profilaxia e o controle ambiental e a intervençao com imunoterapia precoce.


Subject(s)
Humans , Asthma/therapy , Hypersensitivity/therapy , Immunotherapy , T-Lymphocytes/immunology , Asthma/immunology , Autoimmunity/physiology , Causality , Environmental Monitoring , Risk Factors , Time Factors
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