Lymphocyt cytotoxic

ADM may evolve over several years, the extent of fiber atrophy provides an important indication of the chronicity of muscle degeneration. Acute muscle necrosis and phagocytosis give some indication as to how active the disease is at the time of biopsy. In most biopsies from ADM patients, the inflammatory cell foci are perivascular and perimysial rather than endomysial and are dominated by B-lymphocytes. The ratio of T4 lymphocytes (helper cells) to T8 lymphocytes (cytotoxic) generally indicates a predominance of the former. As in JDM, this is consistent with humoral mechanisms of cell damage, and vascular involvement is also apparent in the form of capillary endothelial cell abnormalities (tubular arrays) and duplication of basal lamina. Loss of myofibrillar ATPase from the central portions of fibers is a common prelude to muscle necrosis. 

Seinen W, Vos JG, van Spanje I, Snoek M, Brands R, Hooykaas H (1977a) Toxicity of organotin compounds. II. Comparative in vivo and in vitro studies with various organotin and organolead compounds in different animal species with special emphasis on lymphocyte cytotoxicity. Toxicology and Applied Pharmacology, 42(1) 197-212. 

SOD ha T cell Tc TcR TGA Th TLC TMP/SMX TNF Ts TX U V domain VLA Ml H m superoxide dismutase half-life thymus-derived lymphocyte cytotoxic T cell T-cell receptor thymine-guanine-adenine T helper cell thin layer chromatography trimethoprim/sulphamethazole tumour necrosis factor T suppressor cell thromboxane unit variable domain very-late antigen microlitre (10 6 litre) micrometre (10"6 metre)... 

Stimulation of Fas and TNF-1 receptors directly activates caspases 2 and 8, but Fas ligands can also activate Bid and so cause the mitochondria to enter the apoptotic process. T lymphocytes (cytotoxic lymphocytes) express the Fas ligand and so can cause activation of the Fas-caspase system in target cells. 

Lymphocyte. Bone marrow-derived cell with little cytoplasm, with the ability to migrate and exchange between the circulation and tissues, to home to sites of antigen exposure, and to be held back at these sites. The only cells that specifically recognize and respond to antigens (mainly with the help of accessory cells). Lymphocytes consist of various subsets differing in their function and products (e.g. B lymphocytes, helper T lymphocytes, cytotoxic T lymphocytes, regulatory T cells). 

G19. Granger, G. A., and Williams, T. W. Lymphocyte cytotoxicity in vitro. Activation and release of a cytotoxic factor. Nature (London) 218, 1253-1255 (1968). 

Aldesleukin causes an enhancement of lymphocyte mito-genesis and stimulation of long-term growth of human IL-2-dependent cell lines. It produces an enhancement of lymphocyte cytotoxicity induction of killer cell (lymphokine-activated [LAK] and natural [NAK]) activity induction of interferon-gamma production. 

Sinkovics JG, Cabiness JR, Shullenberger CC. Disappearance after chemotherapy of blocking serum factors as measured in vitro with lymphocytes cytotoxic to tumor cells. Cancer. 1972 30 1428-37. 

Chen HW. Role of cholesterol metabolism in cell growth. FedProc 1984 43 126-130. Dabrowski MR Peel WE, Thomson AE. Plasma membrane cholesterol regulates human lymphocyte cytotoxic function. Ear J Immunol 1980 10 821-827. Ostaszewski P, Kostiuk S, Balasinska B, Jank M, Papet 1, Glomot F. The leucine metabolite 3-hydroxy-3-methylbutyrate (HMB) modifies protein turnover in muscles of the laboratory rats and domestic chicken in vitro. J Anim PhysiolAnim Nutr (Swiss) 2000 84 1-8. 

Vose, B.M. and G.C. Moudpl. 1976. Post-operative depression of antibody-dependent lymphocyte cytotoxicity following minor surgery and anaesthesia. Immunology 30 123-128. 

Gradual diminution of 004 T-lymphocytes from the peripheral blood is the most consistent feature observed in HIV infection. Because the majority of 004 cells are T-helper lymphocytes, removal leads to deficiency of cellular immunity, which depends on T-helper cells to initiate cytotoxic T-ceU killing of vims-infected cells of cancer. The loss of immune surveillance leads to the appearance of viraHy induced tumors from unopposed clonal expansion of viraHy transformed cells. Furthermore, depletion of cellular immunity leads to exaggerated viral, fungal, and proto2oal infections. 

FK-506 (37) interferes with IL-2 synthesis and release and has a cyclosporin-like profile, but is considerably more potent in vitro. IC q values are approximately 100-fold lower. This neutral macroHde suppresses the mixed lymphocyte reaction T-ceU proliferation generation of cytotoxic T-ceUs production of T-ceU derived soluble mediators, such as IL-2, IL-3, and y-IFN and IL-2 receptor expression (83). StmcturaHy, FK-506 is similar to sirolimus. Mycophenolate mofetil (33), brequinar (34), and deoxyspergualin are in various phases of clinical evaluation. Identification of therapeutic efficacy and safety are important factors in the deterrnination of their utiUty as immunosuppressive agents. 

Restricted Cytotoxic T-Lymphocyte Responses," Biomedicine 96 Medical Research from Bench to Bedside, Washiagton, D.C., May 3—6, 1996. 

Leptosins D-F (258a-c, Scheme 39) [94JCS(P1)1859] were isolated by Takahashi and co-workers from the culture of a strain of Leptosphaeria sp. as cytotoxic substances against the P388 lymphocytic leukemia cell line comparable to that of mitomycin C. Utilizing the nucleophilic substitution reaction of 1-hydroxytryptamines, a simple methodology for the synthesis of core structures of leptosins has been developed (2000H1255). 

In this type of reaction an antigen elicits the generation of cytotoxic T-lymphocytes ( immune defense). Cytotoxic T-lymphocytes (Tc) destroy antigen bearing cells by inducing apoptosis. This reaction can be viewed as the cellular counterpart to the humoral Type II reactions. They play an important physiological role in the defense of viruses, and can become allergic reactions under the same conditions as described for Type II reactions. 

For the pathogenesis of multiple sklerosis, autoimmune T-lymphocy tes play a predominant role, which are directed against components of the neural myelin sheath. T-lymphocy tes by secreting cytokines such as interferon y maintain the chronic inflammation which destructs the myelin sheath. Also cytotoxic T-lymphocytes may participate directly. The cause of multiple sklerosis is unknown. Significantly increased antibody titers against several vitusses, mostly the measles virus, point to a (latent) virus infection initiating the disease. 

COPD is a chronic inflammatory disease that results from prolonged and repeated inhalation of particles and gases, chronic (or latent) infection or an interaction of these factors. In many cases, the inflammation persists even when the exposure (in most cases smoking) is stopped. Prominent among the infiltrating leukocytes are neutrophils, CD8+ lymphocytes (Co-receptor for the T-cell receptor. CD8+ is specific for the class IMHC protein. It is expressed on the surface of cytotoxic T-cells and natural killer cells.) and CD68+ monocytic cells (A lysosomal antigen. All cells that rich in... 

Interleukin 2 (Aldesleukin, Proleukin ) is a major growth factor and activator of cytotoxic and other T-lymphocytes. It is applied in the therapy of metastas-ing renal carcinoma and melanoma. Side effects include... 

This class of lymphocytes differentiates from immuno-logically incompetent hematopoietic stem cells of the bone marrow within the thymus - hence, the name thymus-dependent (T-) lymphocytes. Two major subclasses develop simultaneously, T-helper lymphocytes (Th) and cytotoxic effector lymphocytes (Tc). The cytotoxic T-lymphocytes (carrying on the surface the differentiation marker CD8) destroy cells, which cany their cognate antigen bound to MHC class I molecules on the surface by inducing apoptosis. From an evolutionary point of view Tc cells appear to have developed predominantly to cope with vims infections. As vituses can only replicate within cells, Tc eliminate them by destroying their producers. 

Immune Defense. Figure 2 Cytokines involved in the development of adaptive immune responses in secondary lympoid tissues such as the lymph nodes or spleen. Abbreviations B B-lymphocyte, IFN interferon, Ig immunoglobulin, IL interleukin, NK natural killer cell, TE T-effector (cytotoxic) lymphocyte, TH T-helper lymphocyte... 

Several cytokines are in clinical use that support immune responses, such as IL-2, DFNs, or colony-stimulating factors. IL-2 supports the proliferation and effector ftmction of T-lymphocytes in immune compromised patients such as after prolonged dialysis or HIV infection. IFNs support antiviral responses or antitumoral activities of phagocytes, NK cells, and cytotoxic T-lymphocytes. Colony-stimulatory factors enforce the formation of mature blood cells from progenitor cells, e.g., after chemo- or radiotherapy (G-CSF to generate neutrophils, TPO to generate platelets, EPO to generate erythrocytes). 

This is an immunoglobulin fusion protein with the cytotoxic lymphocyte antigen 4 (CTLA-4) receptor. By binding to CD80/86 on APCs it inhibits the CD28 costimulatory signal in lymphocytes. It is speculated that this can result in tolerance but up to now there is only experimental data [3,4]. 

Large granular lymphocytes, not belonging to either the T- or B-cell lineage. Natural killer (NK) cells are considered part of the innate defense system since, in contrast to cytotoxic T-cells, they are able to kill certain tumor cells in vitro without prior sensitization. The basal activity of NIC cells increases dramatically following stimulation with type I IFNs. In addition, NK cells display Fc-receptors for IgG and are important mediators of Antibody-Dependent-Cell-mediated-Cytotoxicity (ADCC). 

Perifascicular capillaries are closer to aggregates of antibody-secreting cells (B-lymphocytes) situated in perimysial connective tissue and therefore are most severely affected by antibody-dependent cytotoxic reactions. Immune-complex deposition occurs at a higher level in the vascular tree (i.e., at arteriolar level) and this may cause fluctuations in perfusion pressure. Perifascicular capillaries are most distal from the head of vascular pressure and therefore most likely to suffer from periodic anoxia. 

The histopathological features of PM may be radically different from those of JDM and ADM. There is little, if any, evidence of involvement of the micro vasculature and the muscle necrosis which occurs appears to be the direct result of targeting of individual muscle fibers. In the dermatomyositis syndromes, antibody-dependent humoral mechanisms are predominant and B-lymphocytes are seen to be the most abundant cell type in almost all JDM cases and a substantial proportion of ADM cases. In contrast, most muscle biopsies from PM patients show evidence of inflammation in which TS (cytotoxic) lymphocytes predominate (Figure 20). Moreover, the distribution of inflammatory cell infiltrates tends to be different. Instead of the mainly perifascicular location of lymphocytes in JDM/ADM, there... 

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