Hungarian Immunology

[Neonatal activation of interferon-γ in macrophages]

ERDŐS Melinda, MARÓDI László

MARCH 20, 2002

Hungarian Immunology - 2002;1(01)

[Each individual passes through developmental or transient immunodeficiency due to the immaturity of the immune system in early childhood, expecially in the neonatal period. Therefore, neonates contract infections by intracellular and extracellular microorganisms more easily than older children and adults, and develop more severe disease with a high mortality rate. A number of abnormalities in the neonate’s host defense systems have been described suggesting that the immune system at birth functionally differs from that in adults. Neonatal T and B cells show decreased reactivity to antigens and mitogens and have deficienct IgM-IgG isotype switching. Newborns have decreased functional capacities of the hemolytic complement system. Under the same in vitro and in vivo conditions neonatal granulocytes show functional deficiency earlier than adult cells. Effector mechanisms of the cell-mediated immunity involve activation of macrophages by T helper1 cytokines, particularly interferon- γ (IFN-γ). IFN-γ is the most important macrophage-activating cytokine in vivo. Neonatal T cells express lower levels of IFN-γ and macrophages are hyporesponsive to activation by this cytokine. This deficiency may be explained by decreased phosphorilation of STAT1 despite comparable expression of STAT1 protein in neonatal and adult macrophages.]



Further articles in this publication

Hungarian Immunology

[In memoriam professor Gyula Petrányi]


Hungarian Immunology

[Anti-inflammatory effects of high-dose intravenous immunoglobulin therapy in immunothrombocytopenic purpura]

ERDŐS Melinda, MARÓDI László

Hungarian Immunology

[2nd C1-esterase inhibitor deficiency workshop, April 2001, Budapest]

FARKAS Henriette, VARGA Lilian, HARMAT György, FÜST György

Hungarian Immunology

[Patomechanism of hereditary angioneurotic oedema and provoking factors of oedematous attacks]

FARKAS Henriette

[The author describes the genetic background of hereditary angioneurotic edema, an autosomal dominant disorder. The pathomechanism of edemaformation and the significance of major mediator substances are explained along with clinical manifestations and their management. A special emphasis is placed on prophylaxis, the mainstay of which is the elimination of precipitating factors. The latter include mechanical trauma, diagnostic and therapeutic interventions performed in the cephalic-cervical region, mental stress, and sex hormones. The effect of endocrine therapies, ACE inhibitors, and infections - Helicobacter pylori in particular - on the natural course of the disease is also discussed.]

Hungarian Immunology

[Relevances of anti-CD44 immunotherapy for cellular biology]

GÁL István, GLANT T. Tibor, MIKECZ Katalin

[INTRODUCTION - The CD44 molecule - the physiologic hialuronic acid receptor - is one of key mediators that direct the traffic of leukocytes into inflamed tissues. When applied in animal models of autoimmune arthritis, parenteral anti-CD44 antibody treatment exerts a dramatic antiinflammatory effect, but at high doses also a leukopenic effect. The goal of the present work is to elucidate the cellular basis of these phenomena. METHODS - In this study the authors used Western blot, immunoprecipitation, cell adhesion studies, flow chamber system studies (leukocyte rolling) and fluorescence microscopy following fluorescent labeling of actin cytoskeleton. RESULTS - Adhesion of CD44-expressing leukocytes to immobilized hialuronic acid does not result marked changes in cellular morphology. When incubated on immobilized anti-CD44 antibody, however, these cells spread, reorganize the actin cytoskeleton, and they adhere strongly to the surface. Studying the mechanisms of signal transduction, the authors found that engagement of CD44 with anti- CD44 antibody results in its enhanced association with numerous cytoskeletal regulator proteins, including ezrin, ankyrin, spectrin and focal adhesion kinase, thereby increasing the interaction between the cytoskeleton and the plasma membrane. Strong adhesion of the cells to immobilized anti-CD44 also prevents the rolling movement of these cells, mediated by CD44-hialuronic acid interactions, which precedes the extravasation of leukocytes to sites of inflammation. CONCLUSION - These results may provide insight into the antiinflammatory mechanisms of anti- CD44 antibody treatment. Based on these results and results published by other investigators, anti- CD44 antibodies may be uselful in the immunotherapy of rheumatic diseases.]

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[Introduction - Differential diagnosis of neonatal and infantile seizures based only on inspection poses a challenge even for specialists. Aims - To investigate the evaluations of neonatal and infantile paroxysmal events based only on inspection. Research question - Is there any difference in the opinion of neonatologists, paediatric neurologists and neurologists about the assessment of common paroxysmal events in infancy? Patients and methods - Video recordings about paroxysmal movements of 15 neonates or infants (aged 2 days- 5 months) were displayed for 47 paediatric neurologists, 35 neonatologists and nurses working in Neonatal or Perinatal Intensive Care Units and 43 neurologists. They had to decide without knowing the past medical history or EEG results whether events presented were epileptic or nonepileptic in nature. Results - Answers of neonatologists and paediatric neurologists were correct in 67% of cases (824/1230), no significant difference was found between their results. The largest uncertainty was in the judgement of discrete hand movements and very rapid clonus with epileptic origin, they were judged correctly by only one third of participants. The result of neurologists was only slightly, but not significantly different from that of paediatric neurologists. Conclusion - In most cases, the correct diagnosis of neonatal and infantile paroxysmal events requires video-EEG recording. No significant difference was revealed between the evaluation of neonatologists and paediatric neurologists about the differential diagnosis of movements. The ongoing cooperation of paediatric neurologists and neurologists going back to several decades facilitates the shaping of a common perspective.]

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Interferon-beta (IFN-β) 1a and glatiramer acetate (GA) are first-line therapies for multiple sclerosis (MS) with immunomodulatory effects. We present a patient who developed lymphopenia and tuberculous lymphadenitis under treatment with these agents. The female patient who at present 65 year old is followed at our MS outpatient clinics had received GA (20 mg/day, subcutaneous injection) and later IFN-β 1a (44 µg, thrice weekly, subcutaneous injection). During the course of her treatment, she developed mild to severe lymphopenia. A follow up thoracic spinal MRI (when lymphocyte count was 800/µl) showed multiple enlarged lymph nodes in the posterior mediastinum incidentally. Further investigation revealed tuberculous lymphadenitis. She received anti-tuberculosis (TB) treatment for nine months and her condition resolved. Although immunomodulatory treatments are considered safe with regard to opportunistic infections, and lymphopenia under these treatments are generally accepted as mild and asymptomatic, our experience was different with this patient. Further studies on the management of patients with lymphopenia and assessment of the risk of TB under immunomodulatory agents are needed.

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Clinical Neuroscience

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