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1

The significance of Treg cells in defective tumor immunity

100%
Kosmaczewska A., Ciszak L., Potoczek S., Frydecka I.
Archivum Immunologiae et Therapiae Experimentalis
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2008
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vol. 56
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issue 3
181-191
EN
Regulatory T cells (Treg) enriched in FoxP3+, glucocorticoid-induced TNF receptor+, and cytotoxic T-lymphocyte-associated antigen-4+ exert a potential to suppress effector T cells in the periphery. These cells exist in markedly higher proportions within tumor-infiltrating lymphocytes, peripheral blood lymphocytes, and/or regional lymph node lymphocytes of patients with cancer and their frequencies are suggested to be strongly related to tumor progression and inversely correlated with the efficacy of treatment. Tumor-specific Treg cells require ligand-specific activation and cell-to-cell contact to exert their suppressive activity on tumor-specific effector cells (CD8+ cytotoxic T lymphocytes and CD4+ Th cells), which includes decreased cytotoxity, proliferation, and Th1 cytokine secrection. Depletion or blockade of Treg cells can enhance immune protection from tumor-associated antigens that are expressed as self antigens. Recent studies revealed that lymphoma T cells might adopt a Treg profile as well. Studies assessing the influence of chemotherapy on Treg cells have also been included in this review.
2

Expression and functional significance of CTLA-4, a negative regulator of T cell activation

100%
Kosmaczewska A., Ciszak L., Bocko D., Frydecka I.
Archivum Immunologiae et Therapiae Experimentalis
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2001
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vol. 49
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issue 1
39-46
EN
The generation of an effective immune response involves antigen-specific T cell expansion and differentiation of effector function. T cell activation requires at least two distinct signals, including signaling via the Ag-specific TCR and a costimulatory pathway. Antigen stimulation of T cells can lead either to a productive immune response characterized by proliferation, differentiation, clonal expansion and effector function or, in absence of appropriate costimulation, to a state of long-lasting unresponsiveness termed anergy. Anergic T cells fail to proliferate and secrete cytokines in response to secondary stimulation. The interaction between costimulatory molecule CD28 on T cells with members of the B7 family on APC results in upregulation of T cell proliferation, cytokine production and induces the expression of the anti-apoptotic protein Bcl-xl. Based of those findings, the two-signal requirement model for T cell activation is today generally accepted. The negative regulatory mechanisms during T cell activation are not well understood, but they are crucial for the maintainance of lymphocyte homeostasis. For several years the functional role of the enigmatic CD28 homologue CTLA-4 (cytotoxic T lymphocyte antigen-4) in T cell activation has been both obscure and conteroversional. CTLA-4 was initially proposed to provide a costimulatory signal in conjunction with TCR/CD3 signaling. Today we know that CD28 and CTLA-4 molecules may have diametrically opposed functions: signaling via CD28, in conjunctive with TCR, is required for T cell activation, while signaling via CTLA-4 is a negative signal that inhibits T cell proliferation. How the T cell integrates signals through the TCR/CD3 complex, CD28 and CTLA-4 to initiate, maintain and terminate antigen-specific immune response is actually not fully clarified. In this review, we will focus on the emerging role of CTLA-4 as a negative regulator of T lymphocyte activation and its role in dynamic interplay of activatory and inhibitory signals.
3

Alterations in the expression of signal-transducing CD3? chain in T cells from patients with chronic inflammatory/autoimmune diseases

88%
Ciszak L., Pawlak E., Kosmaczewska A., Potoczek S., Frydecka I.
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2007
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vol. 55
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issue 6
373-386
EN
The CD3 zeta chain, a component of the T cell receptor (TCR)/CD3 complex, is considered to be a limiting factor in the assembly and transport of the TCR/CD3 complex to the cell surface and is crucial to receptor signaling function. Recent studies have demonstrated altered expression and function of this signal transduction molecule in T and natural killer cells in patients with chronic inflammatory/autoimmune diseases. In this review, current knowledge concerning the expression of CD3 zeta chain as well as the mechanisms responsible for abnormal expression of this molecule in systemic lupus erythematosus, rheumatoid arthritis, and childhood idiopathic nephrotic syndrome are summarized.
4

CD28 costimulatory molecule - expression, structure and function

88%
Bocko D., Kosmaczewska A., Ciszak L., Teodorowska R., Frydecka I.
Archivum Immunologiae et Therapiae Experimentalis
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2002
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vol. 50
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issue 3
169-178
EN
T cell activation is a key event triggering an antigen specific immune response of the organism. The process is induced primarily by signal generated by direct interaction of T cell receptor (TCR) with antigen bound to major histocompatibile complex (MHC) on antigen presenting cell (APC). Although the signal is critical to excite immune response, however additional, costimulating signal is required. The major second signal is generated by interaction of CD28 molecule expressed on most T lymphocytes with its natural ligands CD80 and CD86 located on APCs. Signal excited by CD28 triggering involves multiple second messenger cascades, leading to activation of transcription factors and finally results in cell proliferation, cytokine production, and generation of effector function. The importance of CD28-delivered costimulatory signals was proven in experiments with CD28-deficient mice. T cells from these mice exhibit, impaired pattern of cytokine secretion, defects in T cell dependent antibody production. Certain forms of immunopathology might result from the aberrant regulation of CD28 expression.
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