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Tissue lymphocytes

Produced by lymphoid tissue. Lymphocytes represent about 20% of the WBCs in adults they have a long life span (sometimes several years). They probably serve as memory cells for the immune system. These mononuclear cells may be small, agranular structures (T and B cells) or large, granular cells (NKCs). Different types of T cells may only be differentiated by their cell-surface markers (CD markers - clusters of differentiation). CD markers are identified using labelling antibodies... [Pg.433]

Structure on red blood cells/other tissues, lymphocytes etc ... [Pg.2123]

Frequently, the EAR is followed by a late phase response 4-6 h later and it is caused by the pulmonary sequestration of eosinophils, neutrophils, mast cells, and T-lymphocytes. This leukocyte recruitment depends on mast cell-derived mediators such as TNFa and various chemokines, as well as on the expression of adhesion molecules on leukocytes (e.g. VLA-4, CD11/18) and vascular endothelial cells (e.g. VCAM-1, ICAM-1, E-selectin). Products of these leukocytes have several functions First, they cause the second phase of bron-choconstriction, mucus secretion, and airway swelling second, they cause tissue destruction third, they launch and entertain the chronic inflammation. [Pg.286]

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]

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... [Pg.615]

This experimental drug is a derivative of myriocin. After phosphorylation FTY720 modulates chemotactic responses and lymphocyte trafficking, leading to reversible lymphocyte sequestration in secondary lymphoid tissues. It is in clinical trials for the treatment of multiple sclerosis. [Pg.620]

The SI Pi receptor and the gradient between lymphatic tissue (low SIP levels) and plasma (high SIP levels) are essential for lymphocyte trafficking. Deletion of S1PX, as well as pharmacological... [Pg.714]

Melanocortin peptides have been proposed as potent modulators of many pathologies including inflammatory (asthma, arthritis) and cardiovascular disease. They have been shown to be directed against resident cells within tissue such as macrophages, endothelial cells and also circulating leukocytes (neutrophils and lymphocytes). Therefore harnessing their therapeutic potential could lead to the development of novel therapeutics. [Pg.752]

This complex contains 11 polypeptide subunits of which only one is encoded by mtDNA. Defects of complex III are relatively uncommon and clinical presentations vary. Fatal infantile encephalomyopathies have been described in which severe neonatal lactic acidosis and hypotonia are present along with generalized amino aciduria, a Fanconi syndrome of renal insufficiency and eventual coma and death. Muscle biopsy findings may be uninformative since abnormal mitochondrial distribution is not seen, i.e., there are no ragged-red fibers. Other patients present with pure myopathy in later life and the existence of tissue-specific subunits in complex III has been suggested since one of these patients was shown to have normal complex 111 activity in lymphocytes and fibroblasts. [Pg.311]

Muscle biopsy is usually undertaken to confirm the provisional clinical diagnosis. Because the skin lesions normally precede those in muscle, biopsies of muscle taken early may show little abnormality. Inflammatory foci may be scanty or absent and muscle fiber diameters may be normal. However typical biopsies show discrete foci of inflammatory cells, with a predominance of B-lymphocytes (see Figure 18). These cells are situated in perimysial connective tissue rather than in the en-domysium and are often also perivascular in location. Muscle fiber necrosis occurs in JDM but muscle fibers do not appear to be the primary target of the disordered immune process. Rather, it is the micro vasculature of the muscle which appears to degenerate first and muscle necrosis is preceded by capillary necrosis, detectable at the ultrastructural level. [Pg.327]

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. [Pg.327]

Various syndromes associated with hypereosinophilia involve skeletal muscle. There is a rare form of polymyositis which is characterized by this feature (defined as exceeding 1,500 eosinophils/mm for at least six months). Clinical presentation includes skin changes, heart and lung involvement, and peripheral neuropathy as well as proximal myopathy. The condition must be distinguished from trichinosis and other parasitic infections associated with hypereosinophilia. Muscle biopsy findings are interstitial and perivascular infiltrates in which eosinophils predominate but are accompanied by lymphocytes and plasma cells, and occasional muscle fiber necrosis. Fascitis may also be associated with hypereosinophilia (Shulman s syndrome). This condition is characterized by painful swelling of skin and soft tissues of trunk and extremities and weakness of limb muscles. Biopsy of muscle... [Pg.336]


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See also in sourсe #XX -- [ Pg.16 ]




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