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Costimulatory molecules

Antigen-presenting cells (APCs) are cells of the immune system that are able to process and present foreign antigens to effector cells. The antigen is presented in the context of an MHC-I or MHC-II molecule on APCs in the presence of so-called costimulatory molecules to activate the effector cells. [Pg.134]

In the specialized environment of secondary lymphoid tissues such as lymph nodes or spleen, dendritic cells provide the requirements for naive T-lymphocytes to become activated and to proliferate. The professional antigen-presenting cells present peptides in MHC II, express costimulatory molecules, and release cytokines into the immunological synapse, which is formed by the antigen-presenting cell and the naive T-lymphocyte. Thus, cells of innate immunity initiate and facilitate the activation of naive lymphocytes, and it is easily conceivable that their cytokines and adhesion molecules will instruct the naive T-lymphocyte during activation and differentiation to T-effector cells. [Pg.614]

In addition to its classical role as regulator of calcium homeostasis, 1,25-dihydroxy vitamin D3 (calcitriol) displays immunosuppressive properties. Inhibition of T-lymphocyte proliferation seems to be mediated via regulation of CD80/86 costimulatory molecule expression on APCs. For clinical use as immunosuppressant, however, analogues of vitamin D3 that do not influence calcium metabolism are needed. [Pg.620]

The activation of DRF-3 through the TREF dependent pathway allows for chemokines such as RANTES to be produced. It also leads to the production of DFN-a and EFN-(3, which are involved in anti-viral immunity. The TREF pathway, activated by either TLR-3 or TLR-4, can also induce MHC class-II expression and costimulatory molecules, thus leading to T-cell activation. This provides an important link between innate and adaptive immunity. [Pg.1210]

Data shown are representative of three independent experiments. Cytokine concentrations are in ng/ml. Expression of costimulatory molecules and LDL uptake is represented as Mean Channel Fluorescence. Data represent mean SEM., p < 0.05 for the comparison of untreated and NotoG-treated BMDC, or untreated and LDL-treated BMDC. [Pg.191]

Furthermore, in a recent study by Takei and colleagues, the ginsenoside metabolites Ml (Compound K) and M4 (20(S)-Protopanaxatriol) were demonstrated to promote the maturation of human monocyte-derived DCs [48], M4, and to a lesser extent Ml, increased the DC expression of key costimulatory molecules, decreased their endocytic activity, and induced their production of IL-12. Moreover, these effects had the end result of generating mature DCs that could induce potent Thl polarization. Unfortunately, it was not clearly defined in this study if the ginsenoside metabolites were used at physiologically relevant concentrations, a variable that would be expected to have significant implications on the interpretation of these results. [Pg.191]

Maturation Status of Dendritic Cells Is Critical for Induction of Regulatory T Cells Dendritic cells (DCs) have long been regarded as key cells for the induction of immunity and are defined as natures adjuvants [1]. However, these function(s) are only assigned to DCs after proper maturation. Fully matured DCs express a multitude of MHC and other T-cell costimulatory molecules, which enable them to induce immune reactions. In contrast, non-activated tissue resident DCs have been shown not to possess these T-cell-stimulating capacities [1]. For this reason they were regarded as immature precursors that later become a real and fully developed DC after activation. [Pg.29]

Although closely related, monocytes/macrophages (MO) possess features that are distinct from DCs. Due to their limited expression of T-cell costimulatory molecules, MO are not able to prime T cells de novo, but rather stimulate effector/memory T cells by the secretion of cytokines, which support T-cell proliferation. As DCs, MO differentiate from myeloid precursors and form a heterogeneous population of antigen-presenting cells (APCs) that link the innate and adaptive immune systems. However, their ability to interact with T cells via MHC class II TCR interaction(s) as well as engagement of T-cell costimulatory receptors on their surface, makes close contact between MO and Tregs likely to occur in vivo. [Pg.32]

Except for CD40, NK cell subsets showed different expression of killer-inhibitory receptors and costimulatory molecules between the polyal-lergic and healthy subjects. The study demonstrates that human NK cells comprise distinct receptor-expressing and cytokine-producing subsets similar to Thl and Th2 cells. These subsets of NK cells show differences in surface KIR receptors and costimulatory receptors and interfere with immunoglobulin regulation [34]. [Pg.55]

Nakae S. Suto H, Iikura M, et al Mast cells enhance T cell activation importance of mast cell costimulatory molecules and secreted TNE J Immunol 2006 176 2238-2248. [Pg.66]

Mechanisms involved in UV-B-induced immune tolerance are multiple. UV-B irradiation strongly affects the viability and function of skin DCs [6]. UV-B irradiation causes DNA damage and apoptosis in LCs, while promoting their migration to regional lymph nodes [7]. This effect is paralleled by the reduced expression of MHC and costimulatory molecules, which results in an impaired antigen presenting capability. The release of IL-10 by resident skin cells, ker-atinocytes and mast cells, also contributes to dampen DC function [8, 9]. Thus, upon UV-B irradiation, immature or partially mature DCs,... [Pg.94]

Silva SR. Jacysyn JF. Macedo MS. Faquim-Mauro EL Immunosuppressive components of Ascaris suum down-reg-ulate expression of costimulatory molecules and function of antigen-presenting cells via an IL-10-mediated mechanism. Eur J Immunol 2006 36 3227-3237. [Pg.123]

LL-37 has been demonstrated to affect DC differentiation from monocytes. Thus, monocytes primed with LL-37 demonstrated upregulated phagocytic capacity, and when induced to differentiate to DCs exhibited increased costimulatory molecule expression, enhanced Thl-cytokine production, and improved ability to activate Thl-polarized T-cell immunity. A subsequent investigation by Kandler et working with... [Pg.198]

It is noteworthy that MHC class I downregulation is not the only escape mechanism available for tumors to avoid T cell responses other mechanisms such as downregulation of the tumor antigens, alterations of the apoptosis program, expression of inhibitory molecules, lack of expression of costimulatory molecules leading to immunological tolerance have been also described. The identification of defined immune escape mechanisms in human or mouse tumors point to the existence of active immunosurveillance which is important for the implementation T cell-based immunotherapy protocols. This information will further help to select patients suitable for such therapies. Furthermore, restoration of the tumor MHC class I phenotype to a normal MHC phenotype may be an other strategy to restore an efficient immune response in cancer patients. All these approaches are still hypothetical and no clinical procedures have been tested so far. [Pg.178]


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See also in sourсe #XX -- [ Pg.392 ]




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