Subject(s)
Animals , Humans , Major Histocompatibility Complex/immunology , Acute Disease , Antigen Presentation/immunology , Antigens/immunology , Chronic Disease , Cell Adhesion Molecules/physiology , Cytokines/physiology , Endothelial Cells/cytology , Graft Rejection/immunology , Graft Rejection/pathology , Histocompatibility Antigens/chemistry , Histocompatibility Antigens/immunology , Immunity, Cellular , Leukocytes/cytology , Major Histocompatibility Complex/genetics , T-Lymphocyte Subsets/immunology , Transplantation ImmunologyABSTRACT
Blood transfusion may lead to the manifestation of anti-HLA and platelet-specific antibodies that may in turn bring about different problems like platelet refractoriness. It appears that the study of antibodies against HLA-Class I and platelet-specific antigens are useful for the selection and success of the appropriate treatment protocol. The aim of this study was to detect anti-HLA and anti-platelet-specific antibodies by flowcytometry in patients with hematologic disorders [including Acute Leukemia, Aplastic Anemia] and patients with ITP. In this descriptive study, anti-HLA and platelet-specific antibodies were detected by flowcytometric technique, using 62 sera drawn from patients with different hematological disorders who showed a poor response to platelet transfusion and 20 from patients with ITP. The results of anti-HLA antibodies were then compared by Panel Reactive Antibodies [PRA]. Our results showed 44 [53.7%] out of 82 patients had anti-HLA Class-I antibodies in their sera. The frequency of each antibody isotype was found to be as follows: IgM [51.2%], IgG [32.9%] and IgA [1.2%]. 36 [43.9%] out of 82 patients had platelet specific antibodies and the frequency of each antibody isotype was found to be as follows: IgM [40.2%], IgG [30.5%] and IgA [12.2%]. 27 [31.7%] out of 82 patients had both antibodies. No difference was found between the two groups in platelet specific antibodies. Despite significant correlation between flowcytometry and PRA methods, PRA can only detect antibodies which react with complement. With increase in the number of platelet transfusion, immunization to HLA antigens occures; moreover, immunization against platelet specific antigens may also occure during autoimmunity. The presence of these antibodies may be one of the reasons of poor response to platelet transfusion and platelet refractoriness in patients under study. Conducting similar studies with higher number of samples, platelet cross-match, and the use of HLA- matched platelets for these patients are recommended
Subject(s)
Humans , Histocompatibility Antigens/immunology , Antigens, Human Platelet/immunology , Platelet Transfusion , Antibodies , Flow CytometryABSTRACT
Aunque en la literatura médica existen múltiples publicaciones acerca de la patogenia de la fibrosis intersticial pulmonar (FIDP), estas representan sólo hipótesis que no han aclarado de manera suficiente los mecanismos íntimos de producción del padecimiento. Ante la posibilidad de que estos mecanismos pueden conducir hacia alteraciones inmunológicas capaces de generar la FIDP, varios autores han enfocado el estudio hacia posibles determinantes genéticos que predisponen al padecimiento. En este trabajo presentamos los resultados obtenidos después de analizar pacientes con FIDP y personas sanas en cuanto a antígeno mayor de histocompatibilidad DR y ABC con el fin de poder identificar un antígeno que sea capaz de servir como un marcador para identificar la FIDP. Concluimos que es posible la existencia de un "gen productor de fibrosis" aunque se requiere de una muestra más numerosa para corroborar nuestros resultados
Subject(s)
Humans , Adult , Histocompatibility Antigens/immunology , Histocompatibility Antigens , HLA Antigens/analysis , HLA Antigens/blood , Pulmonary Fibrosis/immunology , Pulmonary Fibrosis/physiopathologySubject(s)
Humans , Asthma/physiopathology , Bronchial Hyperreactivity/physiopathology , Bronchi/physiopathology , Histocompatibility Antigens/adverse effects , Histocompatibility Antigens/immunology , Asthma/immunology , Bronchial Hyperreactivity/pathology , Bronchi/anatomy & histology , Bronchi/metabolism , Cytokines/adverse effects , Cytokines/immunology , Eicosanoids/adverse effects , Eicosanoids/immunology , Epithelium/pathology , Epithelium/physiopathology , Extracellular Matrix/pathology , Proteoglycans/adverse effects , Lung/anatomy & histology , Lung/physiopathologySubject(s)
Humans , Gastrointestinal Diseases/genetics , Liver Diseases/genetics , Histocompatibility Antigens/immunology , Gastrointestinal Diseases/etiology , Gastrointestinal Diseases/physiopathology , Gastrointestinal Diseases/prevention & control , Genetic Techniques , Liver Diseases/immunology , Liver Diseases/therapySubject(s)
Histocompatibility Antigens/immunology , Autoimmunity , Hypersensitivity, Delayed/immunology , Immune System/physiology , Immunity, Cellular , Inflammation/immunology , Bone Resorption/immunology , Antigen-Antibody Reactions/immunology , Cytokines/immunology , Phagocytosis/immunology , Bone Regeneration/immunologyABSTRACT
Os antígenos protéicos säo degradados em peptídios ao nível intracelular e apresentados às moléculas do sistema maior de histocompatibilidade (MHCI e II). A via MHCI é endógena e a MHC II. exógena. O MHCI é responsável pela ativaçäo celular citotóxica do linfócito T. O MHCII através da interaçäo com os receptores de células T(TCR) induz os linfócitos T belper a produzirem linfocinas ativadoras dos linfócitos B para a sua diferenciaçäo terminal em células secretoras de anticorpos específicos. A seletividade de expressäo antigênica celular das moléculas do MHCII constitui um fator de restriçäo ao surgimento de auto-anticorpogênese
Subject(s)
Humans , Antigens/immunology , Major Histocompatibility Complex/immunology , T-Lymphocytes/immunology , Antigen-Presenting Cells/immunology , Histocompatibility Antigens/immunologySubject(s)
Humans , Animals , Mice , Rabbits , Graft Rejection/immunology , Histocompatibility Antigens/immunology , Genes, MHC Class I/immunology , Immunotherapy , Cell Adhesion Molecules/immunology , Receptors, Cell Surface/immunology , Receptors, Interleukin-2/immunology , Graft Rejection/therapyABSTRACT
Presence of alloantigens on various murine tumors was tested by tumor rejection in allosensitized Swiss mice. The results indicated the presence of alloantigen on immunogenic tumors like chemically induced fibrosarcoma (FS), ascitic sarcoma 180 (S 180) and immunogenic variant of lymphosarcoma (LS-A) in Swiss mice, while these antigens could not be detected by this procedure on spontaneous lymphosarcoma (LS). Allosensitization with skin graft was found to offer quantitatively higher antitumor resistance than the allosensitization achieved by allogeneic lymphocytes. Antitumor effect was not seen when tumor cells were inoculated earlier than day 3 of grafting. Further, host immunosuppression with whole body irradiation up to day of 3 of skin grafting abrogated the antitumor effect. H-2 compatible and non-H-2 incompatible skin graft sensitization of host could offer resistance against both S 180 and LS-A. Further, tumor immune mice rejected H-2 compatible, non-H-2 incompatible skin graft significantly earlier.
Subject(s)
Animals , Antigens, Neoplasm/immunology , Graft Rejection/immunology , Histocompatibility Antigens/immunology , Immunization/methods , Immunotherapy, Adoptive , Isoantigens/immunology , Mice , Mice, Inbred Strains/immunology , Neoplasm Transplantation , Neoplasms, Experimental/immunology , Skin Transplantation/immunology , Transplantation, Homologous/immunology , Whole-Body IrradiationABSTRACT
Se investigó la existencia de influencias parentales que pudieran afectar el recononcimiento de los antígenos de histocompatibilidad propios en la progenie. Se pudo observar que 1) tanto las células de hígado fetal como los esplenocitos y timocitos de hbridos F1 recién nascidos diferen en su capacidad de regular las reacciones alorreactivas parentales dirigidas a antígenos de histocompatibilidad propios según éstos sean de origen materno o paterno. Son capaces de suprimir - hasta el día 5 después del nacimiento- las reacciones sistémicas y locales de GvH inducidas con células maternas mientras que no suprimen aquellas desencadenadas con células paternas; 2) la falta de actividad supresora correlaciona con la aparición de células tímicas con actividad contrasupresora; 3) los esplenocitos de híbridos F1 adultos recíprocos diferen significativamente en su capacidad para estimular la proliferación de células T en reacciones de cultivo mixto singeneico; 4) el amamantamiento de los híbridos F1 con hembras provenientes de la cepa paterna es capaz de inducir alteraciones permanentes en la capacidad estimulatorra de los esplenocitos; el patrón estimulatorio de los esplenocitos de híbridos anamantados por nodrizas de la cepa híbridos F1 recíprocos adultos diferen en su respuesta a antígenos convencionales presentados en el contexto de los antígenos la parentales, estando la lactancia centralmente involucrada. Se discuten los posibles mecanismos involucrados
Subject(s)
Animals , Male , Female , Mice , Graft vs Host Reaction/immunology , Histocompatibility Antigens/genetics , Immunity, Maternally-Acquired , Spleen/cytology , T-Lymphocytes/physiology , Gene Pool , Histocompatibility Antigens/immunology , Mice, Inbred AKR , Mice, Inbred BALB C , Mice, Inbred DBAABSTRACT
Os antígenos do Complexo Principal de Histocompatibilidade, primeiramente descritos como antígenos de transplantaçäo, têm hoje sabidamente um importante papel biológico nas interaçöes celulares. Neste artigo, säo descritas três abordagem trata do uso dos anticorpos monoclonais e histocompatibilidade, com ênfase no uso dos anticorpos polimórficos dirigidos contra produtos dos genes de classes I e II. A segunda abordagem discutida é a Polimorfismo do Tamanho de Fragmentos de Restriçäo (RFLP - Restriction Fragment Lenght Polimorphism). Seu maior emprego reside na grande resoluçäo que oferece, a nível de DNA dos diferentes antígenos, principalmente os de classe II. A terceira e última abordagem discute o reconhecimento imunoquímico dos antígenos de superficie celular pelo soro de pacientes transplantados, com o uso das técnicas de imunoprecipitaçäo e imunoblot