Hungarian Immunology

[Natural immunity]

SZEGEDI Gyula

JANUARY 30, 2006

Hungarian Immunology - 2006;5(01)

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Further articles in this publication

Hungarian Immunology

[Regional cues and phenotypic responses during the ontogeny and postnatal development of splenic vasculatur]

BALOGH Péter

[Among structured peripheral lymphoid tissues in man and rodents, the spleen demonstrates the most extensive flexibility in functional activities, which is coupled with considerable tissue architecture adjustments during ontogeny and immune reactions. The sequential conversion of a primary lymphohemopoietic tissue into a major peripheral lymphoid organ (while participating in the post-myeloid period of primary B-lymphopoiesis and retaining the potential for myelopoiesis) is accompanied with the ordered segregation involving various non-hemopoietic components of architecture, including the endothelia of blood vessels. In this report we will survey the functional and structural aspects of heterogeneous endothelial cells lining the various splenic vascular beds, comprising the complex circulatory network of the spleen. These features will be correlated with the characteristics of those regulatory mechanisms that have recently been demonstrated to be responsible for the establishment and maintenance of the endothelial divergence during splenic vascular development, including crucial transcription factors, morphogenic regulatory ligands and receptors of the tumor necrosis factor/lymphotoxin (TNF/LT) family and others. The influence of these regulatory elements in mice appears to be highly restricted in terms of regional involvement of the vasculature, with cellular alterations of the marginal sinus representing the most frequently affected region. This complexity highlights the importance of this tissue region in both the formation of splenic vasculature and a possible source for white pulp stromal elements as well as its function as a major gateway for lymphocyte traffic.]

Hungarian Immunology

[Primer and transitory defects of interferonactivated pathways]

ERDŐS Melinda, MARÓDI László

Hungarian Immunology

[Mutations of La gene: the proper reaction of the immune system]

SEMSEI Imre

[Numerous hypotheses have emerged to solve the problem and the pathomechanism of autoimmunity so far. Different factors are suspected, from viruses to neuroendocrine elements, to be a pathogen in the etiology of autoimmune diseases. Most of the theories are based on the assumption that something happens to the immune system and it leads to an autoimmune reaction against the proper self. This paper indicates that, at least in certain cases, the immune system reacts properly against the altered cells; therefore the cause of the autoimmunity lies in the other improper functioning of the body. Experimental data show that La autoantigen plays a role not only as a diagnostic marker but it may participate in the pathomechanism of certain autoimmune diseases as well. Mutations in the exon 7 of La gene have such consequences that could lead to the formation of autoimmune reactions detected.]

Hungarian Immunology

[Congress of the American College of Rheumatology, 2005]

SZŰCS Gabriella, SZÁNTÓ Sándor

Hungarian Immunology

[Antiphospholipid syndrome - focused on the childhood form]

KÁLOVICS Tamás, PONYI Andrea, BENSE Tamás, MÜLLER Judit, DANKÓ Katalin, FEKETE György, CONSTANTIN Tamás

[Antiphospholipid syndrome is an autoimmune disorder characterized by recurrent thromboembolic events with concurrent presence of antiphospholipid antibodies in the sera. The morbidity and mortality of the syndrome is defined by the clinical manifestations: deep vein thrombosis, cerebrovascular events, myocardial infarct, pulmonary embolism, recurrent pregnancy losses and prematurity. The authors reviewed the pathogenesis, the clinical course and the treatment of the antiphospholipid syndrome focused on the childhood form.]

All articles in the issue

Related contents

Clinical Neuroscience

[EXAMINATION OF NATURAL COAGULATION INHIBITOR PROTEINS IN THE ACUTE PHASE OF ISCHAEMIC ST]

OLÁH László, CSÉPÁNY Tünde, BERECZKY Zsuzsanna, KERÉNYI Adrienne, MISZ Mária, KAPPELMAYER János, CSIBA László

[Introduction - Decreased activity of natural anticoagulants (antithrombin-III, protein C, protein S) rarely causes cerebral ischaemia, however it can be found frequently in acute phase of ischaemic stroke. The authors’ aim was to investigate whether the decreased activity of natural anticoagulants is accompanied by worsening of symptoms in ischaemic stroke. Patients and method - Sixty-eight acute ischaemic stroke patients were investigated. Severity of symptoms were assessed and followed by the NIH Stroke Scale. Antithrombin- III, protein C, protein S activities, and concentration of C-reactive protein (CRP) were measured within 48 hours after onset of ischaemic stroke. Results - Progressing stroke was found in 29% of patients. Decreased activity of at least one natural anticoagulant proteins was present in 31% of patients. Progression of stroke symptoms occured in 76% of patients with decreased natural anticoagulant activity, while this proportion was only 9% in those with normal natural coagulation inhibitor protein activity (p<0.01). Progressing stroke was also more frequent in patients with elevated CRP value (60%) than in those with normal CRP level (11%; p<0.05). Decreased activity of natural anticoagulants was more frequent in patients with elevated CRP concentration compared with patients with normal CRP. Conclusion - The results demonstrate the importance of decreased activity of natural anticoagulants in acute phase of ischaemic stroke. This abnormality was present in about 1/3 of stroke patients. The decreased activity of natural coagulant inhibitor proteins may play an important role in development of progressing stroke thus indicating unfavourable outcome.]

Clinical Oncology

[Viral infections during oncotherapy ]

ARÁNYI Zsuzsanna

[Immunosuppressive therapies, which were used in the past few years, have been causing different kinds of immunosuppression. In case of impaired cellular immunity, there is an increased risk of having the reactivation of latent viral infections. Certain viral infections or viral reactivations can be life threatening for patients with malignant diseases. Mild viral infections during chemotherapy can also disadvance the tumor therapy, which could affect the chance of recovery in a negative way. This is the reason, why the possibility of carrying viral infections or viral reactivations should be taken into consideration even in patients with solid tumor. Due to this, risk adaptive prevention strategies, and in certain cases, early antiviral therapies are needed.]

LAM Extra for General Practicioners

[Secondary hyperaldosteronism resulting from a feeding disorder]

TÓTH Géza, RÁCZ Károly, FŰTŐ László

[INTRODUCTION - A number of diseases can cause hyperreninaemia and secondary hyperaldosteronism due to the stimulation of the renin-angiotensin system (RAS). The authors present a case of a patient suffering from a feeding disorder, whose secondary hyperaldosteronism verified by hormone examinations recovered after resolution of the feeding disorder. CASE REPORT - The authors found that the patient, who had been on an extreme vegetarian diet and avioded all forms of common salt as well as natural sodium intake for 8 years, had consistently normal electrolite levels, normal blood pressure, elevated plasma renin activity (PRA) and plasma aldosterone levels. Salt loading and postural tests verified secondary hyperaldosteronism. All known diseases that might lead to elevated RAS activity were excluded. After cessation of the salt-restricted diet, the patient’s PRA and plasma aldosteron levels returned to the normal range, which confirmed the possibility that the secondary hyperaldosteronism developed because of the feeding disorder. CONCLUSION - The authors have not found similar hormon alterations due to alimentary causes in humans in the literature. According to their hypothesis, the feeding disorder might lead to secondary hyperaldosteronism via affecting the system or systems that regulate RAS activity.]

Lege Artis Medicinae

[CURRENT PRACTICAL VACCINOLOGY]

JELENIK Zsuzsanna

[The author deals with the current situation and new trends of vaccinology by focusing on the interests of practitioners. The main topics are the changes of antigens (such as pertussis, measles, or poliomyelitis) to provide better efficacy and milder reactogenity or less adverse events. Purifying the vaccines, like thiomersal and human proteins free vaccines is another proven method to achieve better safety. New antigens e.g. Rota, Lyme, meningococcus B are in the pipeline of vaccinology. The aim of producing a combined vaccine is to achieve immunity against more diseases with less inconvenience for the patient, while achieving higher vaccine coverage (DPT-Hib-HBV-IPV). The epidemiological and clinical experiences will influence the current vaccine schedule such as revaccinations of MMR, and remove the need for revaccinations of BCG and hepaB. The special target groups of immunizations are the elderly and patients with chronic disease. Groups of specialists are working on the vaccine recommendation guidelines for certain risk groups. At the same time, with the successful eradication of polio in Europe the practitioners now have to face the antivaccination movement, as well. The main tools to convince people about the benefit of vaccinations are health education and information.]

Hungarian Immunology

[On the role of aging in etiology of autoimmunity]

SEMSEI Imre, ZEHER Margit, BAKÓ Gyula

[Several types of diseases, among others autoimmune illnesses, could be coupled with the general processes of aging. The two-edged sword of the immune defense is directed once against environmental attacks and on the other side against the self. However, one has to make a difference between normal (physiological) clearance and autoimmune diseases, although both sides of autoimmunity are influenced by the general processes of senescence. Aging of the thymus seems to be one of the key elements of the etiology of autoimmunity, although other cell types and their aging also play a substantial role in this process. The spontaneous genetic instability, the acquired genetic mutations due to aging and the age-related alterations of the information level of the body together may be important elements of the patomechanism of both the physiological autoimmunity and the autoimmune diseases. Nevertheless, physiological autoimmunity seems to be directed mostly by natural factors (such as aging and apoptosis) but primary autoimmune diseases may be caused by genetic instability that is enhanced by aging as well.]