Student Researchers' Society Topics

The bone marrow microenvironment plays an important role in various hematological diseases. This project is about optimizing murine and human bone marrow stromal cell isolation techniques for flow cytometric measurements and potential downstream transcriptomic analyses.

Multiple myeloma cells are malignant plasma cells that reside in the bone marrow and interact with local non-tumor cells. Using a mouse model of myeloma we will investigate the early immune response against myeloma cells.

Co-supervisor: Prof. Dr. BALOGH, Péter, MD PhD

A frequent model for the investigations of B-cell lymphomas relies on the studying of B-cell tumors in mice. We have identified in our department a novel spontaneous murine tumor displaying the characteristics of follicular lymphoma, which shows a preferential spreading via the lymphatic vessels. The aim of this project is to define the tissue partners of lymphoma cells and the signals providing survival stimuli.

A frequent model for the investigations of B-cell lymphomas relies on the studying of B-cell tumors in mice. We have identified in our department a novel spontaneous murine tumor displaying the characteristics of follicular lymphoma, which shows a preferential spreading via the lymphatic vessels. The aim of this project is to define the tissue partners of lymphoma cells and the signals providing survival stimuli.

Cytokines play a critical role in the pathogenesis of autoimmune diseases through their diverse functions and complex interactions. Anti-cytokine autoantibodies further modulate immune responses by regulating the availability and activity of cytokines. Although anti-cytokine autoantibodies are also present in healthy individuals, their levels may be altered in patients with autoimmune diseases. In systemic sclerosis, a complex autoimmune disease characterized by fibrosis and vascular abnormalities, these autoantibodies may influence disease progression and severity. Investigating their presence and correlation with clinical parameters helps to better understand the underlying mechanisms and to identify new potential therapeutic targets.

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Systemic sclerosis (SSc) is a chronic connective tissue disease characterized by vascular damage and consequent ischemic-reperfusion injury and multiorgan fibrosis. Dysregulation of the immune system is one of the hallmarks of SSc and B cell phenotypic alterations and activation accompanied by the production of disease-specific autoantibodies, secretion of pro-inflammatory and pro-fibrotic cytokines and direct cooperation with fibroblasts and T cells contribute to the development of SSc. The anti-CD20 monoclonal antibody therapy seems to show some clinical efficacy in SSc further emphasizing the importance of B cells in the development of the disease. Detailed analysis of B lymphocytes of patients with different forms and stages of systemic sclerosis could contribute to the better understanding of the pathomechanism of the disease, and may identify new biomarkers for assessment of disease activity, determination of disease subsets, and prediction of prognosis. The results of these studies may also be directly used to develop new diagnostic tools and therapeutic approaches targeting abnormal B-cells, which can advance medical treatment and lead to better care for affected patients.

Adipose tissue is best known for its roles in metabolism and energy storage. However, growing evidence suggests that it also contributes to a range of immunological processes. To study the interplay between the immune system and adipose tissue, we employ flow cytometry and advanced microscopy techniques in mouse models.

Co-supervisor: Prof. Dr. BALOGH, Péter, MD PhD

Homing of regulatory T cells to the intestine is an important step in the development of tolerance against orally administered antigens (e.g. food proteins and commensal microbiota).  Homing to the intestine is mainly mediated by MAdCAM-1.  The object of the research is to investigate the effect of the absence of MAdCAM-1 on the inducibility of oral tolerance using various knockout mouse models.

Co-supervisor: Dr. BÖRÖCZ, Katalin

Type I interferons (IFN) play a major role in the pathogenesis of many autoimmune diseases, including systemic sclerosis (SSc). Type I IFNs are involved in the regulation of several B cell functions such as antigen presentation, differentiation, antibody, cytokine production and B cells are known to play a key role in the pathogenesis of SSc, in particular through their production of pathological autoantibody and pro-inflammatory cytokines. Antibody treatment against type I IFNs is already under clinical trial in SSc. Our studies aim to investigate the contribution of type I IFN signaling to B-cell pathophysiology in SSc, which may help to better understand the pathogenesis of the disease and to discover new potential therapeutic targets.

Co-supervisor: Dr. ERDŐ-BONYÁR, Szabina

A key feature of the immune system is the ability to distinguish the normal self from the non-self or modified-self antigens. While against external antigens the immune system develops offensive immune reactions, the self-antigens are tolerated. In the development of tolerance two mechanisms play key role: i) central tolerance ensures that no autoreactive lymphocytes can get out from the primary lymph organs ii) peripheral tolerance controls the possible autoimmune reactions on the periphery. In general, when any component of the normal tolerance mechanisms fail autoimmune diseases develop. From 5% to 7% of the European and North American population is affected by autoimmune diseases. Rheumatoid arthritis is a systemic autoimmune disease targeting the synovial joints which affects ~1% of the population, and progresses from severe inflammation to deformities and loss of function primarily in the small peripheral joints. Several animal models can mimic one or more characteristics of this human disease, of which cartilage proteoglycan (PG)-induced arthritis (PGIA) in BALB/c mice is a T cell-dependent and B cell/antibody-mediated autoimmune disease. More and more research aims to find therapies based on normalizing the physiological immunological balance and correcting impaired tolerance mechanisms in the hope of long term remission. Numerous experiments have shown that in case of an identified autoantigen, tolerance can be induced by peptide (autoantigen) vaccination, e.g. in the experimental animal models of multiple sclerosis, collagen-induced arthritis, and non-obese diabetic mice. With the autoimmune arthritis model (PGIA) available in our laboratory, we study whether tolerance can be induced by vaccination with the autoantigen in a peptide-nanoparticle complex to ameliorate/eliminate the disease. We analyze the potential cellular and molecular background mechanisms of tolerance induction.

Co-supervisor: Dr. BÖRÖCZ, Katalin

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One of the most ancient immune defense mechanism is the phagocytosis, that can be manifested in different forms. The aim of research is to identify the various phagocytes and describe their functional characteristics with different cellular and molecular immunological methods in intact and regenerating invertebrate model organism.

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Therapeutic depletion of various leukocyte subsets by monoclonal antibodies has become a routine clinical strategy; however, it is not known how its efficiency is modulated by the lymphoid microenvironment the target cells reside in. The aim of this study is to compare the efficiency of anti-T-cell monoclonal antibodies between various peripheral lymphoid tissues using mouse models, and to define how these tissue locations modulate the establishment of resistance against treatment.

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Co-supervisor: Dr. ERDŐ-BONYÁR, Szabina, PhD

Systemic sclerosis is a systemic autoimmune disease affecting the skin and internal organs. B cells play a key role in the pathogenesis of the disease, particularly through their production of pathological autoantibodies and pro-inflammatory cytokines. Besides signals through classic B-cell receptors, molecules of the innate immune system, including Toll-like receptors, can also influence B-cell activation and function. The aim of our studies is to investigate the contribution of signals via Toll-like receptors to the abnormal function of B cells in systemic sclerosis, which may help to better understand the pathogenesis of the disease and discover new potential therapeutic targets.