Hungarian Immunology

[Experimental arthritis model]

SZÁNTÓ Sándor, GONDA Andrea, MIKECZ Katalin, GLANT Tibor, SZEKANECZ Zoltán

FEBRUARY 20, 2005

Hungarian Immunology - 2005;4(01)

[Animal models of experimental arthritis can be used to understand pathophysiology of the arthritic processes in patients and provide opportunity to develop new therapeutic approaches. The animal models can be divided into different categories based on the pathomechanism of the model and on the features that resemble human inflammatory joint diseases. This review provides an overview of the most widely used types of experimental arthritis models emphasizing their advantages and limitations in the basic arthritis research.]



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Hungarian Immunology


Hungarian Immunology

[Immunology delectat]


Hungarian Immunology

[Immune-dysfunctions in patients with Hodgkin’s lymphoma being in a long lasting complete remission]

ALEKSZA Magdolna, KERESZTES Katalin, BARÁTH Sándor, SIPKA Sándor, ILLÉS Árpád

[OBJECTIVES - Immunosuppression has long been known to be associated with Hodgkin’s lymphoma. The authors report on immunologic abnormalities with special focus on cellular immunity in patients with Hodgkin’s disease in complete remission. METHODS - We determined the proportion of the lymphocytes subpopulations, activated T cells, CD4+/CD25+ suppressor T cell population and intracytoplasmic cytokines by flow cytometry. The soluble cytokines were measured by classical ELISA technique. RESULTS - Based on lymphocyte cell surface antigen expression the subpopulations were as described in the literature, however a unique elevation of CD4+/CD25+ cell fraction was detected. The decreased amount of IFN-γ in the serum suggest Th2 dominance, but reduced intracellular IL-4 production in both CD4+ and CD8+ cells results from Th1 dominance. These results somewhat contrary but can not be completely compared as in vivo and in vitro techniques used for the analysis are not identical. However a constant elevation concentration and expression of IL-10 and TGF-β is observed. CONCLUSION - These alterations may reflect the existence of an immunosuppressive state also in the peripheral blood of Hodgkin’s lymphoma patients not only in the lymph nodes.]

Hungarian Immunology

[History of immunology in Hungary Part VI]


Hungarian Immunology

[Pathomechanism of Crohn’s disease and ulcerative colitis]

GÁL István, CSIKI Zoltán, SZEGEDI László, KISS Gyula

[The two archetypes of inflammatory bowel diseases, Crohn’s disease (CD) and ulcerative colitis (UC) have a considerably high prevalence and chronic morbidity, and thereby a striking public health relevance amongst the maladies involving the gastrointestinal tract. Unveiling their pathogenesis can be the key for the development of successful therapeutic approaches. Our view of these diseases has undergone radical changes in the past few years, and the latest discoveries have shed new light upon their pathomechanism. A multifactorial view is appropriate when explaining their pathogenesis, although certain factors are seemingly of particular importance.]

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Hungarian Immunology

[Therapeutic treatment of rheumatoid arthritis by gene therapy-induced apoptosis]

JAMES M. Woods, VOLIN V. Michael

[Gene therapy was initially conceptualized as a treatment for individuals with genetic disorders, where defective genes would be replaced with functional ones. This concept was eventually broadened to include the use of gene therapy as a delivery mechanism for gene products effective in the treatment of diseases. The latter use of gene therapy, essentially as a drug delivery mechanism, was recognized to be particularly useful in the treatment of rheumatoid arthritis because it may have many advantages over traditional therapies. Two groups of target genes that are potentially useful for gene transfer include soluble inflammatory mediators that in theory could suppress the inflammatory process, and apoptotic mediators that may induce cell death, thereby suppressing the accumulation of inflammatory cells in the joint. To date the former group of target genes has received most of the attention, but it is the latter group of apoptosis-inducing targets that will be discussed in this review. We will focus our discussion on target genes that have shown success at inducing apoptosis in animal models of arthritis and will also include discussion of the apoptotic pathways that are altered in the attempts to reduce inflamed synovial tissue.]

Hungarian Immunology

[First experience with rituximab treatment in rheumatoid artritis: a case report of a multiresistant patient]


[INTRODUCTION - Here we describe the case of the first Hungarian rheumatoid arthritis (RA) patient treated with RTX. CASE REPORT - This multiresistant patient had received numerous immunosuppressive drugs and all three anti-TNF agents had been tried. These biologicals had to be stopped due to inefficacy or side effects. RTX treatment resulted in some subjective clinical improvement, as well as a decrease in rheumatoid factor and anti-CCP production. Clinical activity assessed by DAS28 fell after 18 weeks. B cells disappeared from the circulation, however, the percentage of activated T cells increased. We observed initial B cell recovery after 18 weeks. CONCLUSION - Clinical studies suggest that RTX is more effective right after the failure of the first TNF inhibitor. Efficacy of RTX in this patient suggests that this drug may also be effective in a multiresistant patient, who had tried numerous TNF blockers.]


[The pathogenic and clinical significance of the RANK-RANKL-osteoprotegerin system in rheumatoid arthritis]


[Rheumatoid arthritis (RA) is characterised by increased local and generalised bone resorption, which manifests in the develoment of marginal erosions and generalised osteoporosis, respectively. An increasing number of data suggest that lymphocytes, proinflammatory cytokines and other mediators involved in inflammation contribute to arthritic bone resorption. Therefore, the term ‘osteoimmunology’ has also become widely used. In RA, Receptor Activator of Nuclear Factor kappa B (RANK) and its ligand (RANKL) play a crucial role in bone resorption. These proteins, which belong to the tumor necrosis factor a (TNF-a) receptor and TNF ligand superfamilies, respectively, activate osteoclasts while interacting with T cells, synovial fibroblasts and other cytokines (e.g. IL-1, IL-17), which results in bone resorption. Osteoprotegerin (OPG) is a decoy receptor that also belongs to the TNF receptor family and inhibits RANK-RANKL interactions. There is increased RANKL production and decreased OPG production in RA. The interaction of RANKL with IL-17 is particularly important. Regarding therapy, sulfasalazine, methotrexate and biological agents, especially TNF inhibitors suppress RANKL-mediated bone resorption and thus the development of joint erosions. RANKL-RANK interaction can be directly inhibited by recombinant OPG or anti-RANKL antibody (denosumab). Among these agents, denosumab gave promising results in experiments performed in animal models of arthritis. These were followed by a phase II human RA trial, which proved that denosumab decreased MRI erosion scores in RA.]

Lege Artis Medicinae

[Therapeutic strategies in rheumatoid arthritis]


[In this review, we follow the consecutive steps of the internationally accepted therapeutic strategy of rheumatoid arthritis (RA). We summarise in brief the current European recommendations, and provide some advice on methotrexate (MTX) therapy. The initiation, maintenance and, if needed, switch of biological therapy is also discussed. Having reached remission or low disease activity (LDA), tapering or discontinuation of biologics may be considered. Finally, we review the possibilities and the most important biomarkers of personalised treatment.]


[Vitamin D receptor gene BsmI polymorphism in rheumatoid arthritis and associated osteoporosis]

PÁKOZDI Angéla és munkatársai

[Rheumatoid arthritis is frequently associated with secondary osteopenia or osteoporosis. Gene polymorphisms, such as the BsmI polymorphism of the vitamin D receptor gene are likely to be be involved in the pathogenesis of osteoporosis. However, very little information is available on the role of the BsmI polymorphism in rheumatoid arthritis or in arthritisassociated metabolic bone disorders. Here the authors review international data on vitamin D receptor gene polymorphisms and their relationship with bone metabolism.The authors emphasize that more detailed research is needed to clarify the relationship between these polymorphisms and rheumatoid arthritis.]