Clonality

Ultimately a plasmid is defined by its mode of DNA repHcation. DNA repHcation is initiated at a single, characteristic sequence, termed the origin. The origin sequence determines the copy number of the plasmid relative to the host chromosome and the host enzymes that are involved in plasmid repHcation. Two different plasmids that contain the same origin sequence are termed incompatible. This term does not refer to the active exclusion of one plasmid by another from the ceU but rather to a stochastic process by which the two plasmids are partitioned differentially into progeny ceUs. A ceU which contains two plasmids of the same incompatibiHty group segregates two clonal populations, each of which has one of the two plasmids in it. 

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. 

Humanized recombinant anti-IL-2 receptor antibodies (Basiliximab, Simulect , and Daclizumab Zenapax ). These antibodies bind with high affinity to the IL-2 receptor on T-lymphocytes and prevent activation and clonal expansion of anti-allograft T-lymphocytes by endogenous IL-2. They are used to prevent kidney allograft rejection. The main side effect is immunosuppression. 

Substances that cause cells, particularly lymphocytes, to undergo cell division. Mitogens are also referred to as polyclonal activators, since they stimulate proliferation of lymphocytes irrespective of their clonal origin. The best known mitogens are phytohemagglutinines isolated from certain plants. 

Hepatocellular carcinoma (HCC) develops in patients with chronic liver diseases associated with hepatitis B and hepatitis C vims infections with high incidences. Here, an acyclic retinoid has been shown to suppress the posttherapeutic recurrence after interferon-y or glycerrhicin treatment in cirrhotic patients who underwent curative treatment of preceding tumors. The retinoid induced the disappearance of serum lectin-reactive a-fetoprotein (AFP-L3), a tumor marker indicating the presence of unrecognizable tumors in the remnant liver, suggesting a deletion of such minute (pre)malignant clones (clonal deletion). As a molecular mechanism of the clonal deletion, a novel mechanism of... 

Clonal Selection Clostridial Neurotoxins Clostridium Botulinum Toxin Clotting CNTF... 

Kitrinos K, Labranche C, Stanhope M, Madsen H, Demarest J (2005) Clonal analysis detects preexisting R5X4-tropic virus in patient demonstrating population-level tropism switch on 873140 monotherapy. Antivir Ther 10 S68... 

Kustikova OS, Fehse B, Dullmann J, Kamino K, von Neuhoff N, Schlegelberger B, Li Z, Baum C (2005) Clonal dominance of hematopoietic stem cells triggered by retroviral gene marking. Science 308 1171-1174... 

Brittain E, Noel P, Metcalfe DD Demonstration of an aberrant mast-cell population with clonal markers in a subset of patients with idiopathic anaphy- 72 laxis. Blood 2007 110 2331-2333. 

Mast cells express high-affinity IgE Fc receptors (FceRI) on their surface, contain cytoplasmic granules which are major sources of histamine and other inflammatory mediators, and are activated to release and generate these mediators by IgE-dependent and non-IgE-dependent mechanisms [1]. Disturbances either in the release of mast cell mediators or in mast cell proliferation are associated with clonal mast cell disorders including monoclonal mast cell activation syndrome (MMAS) and mastocytosis respectively, which are in turn associated with some cases of anaphylaxis [2], Molecular mechanisms have been identified which may link increased releasability of mast cell mediators and conditions leading to increased mast cell numbers [3]. Patients with mastocytosis have an increased risk to develop anaphylaxis [4, 5] and those with anaphylaxis may suffer from unrecognized mastocytosis or may display incomplete features of the disease [6-8]. 

Systemic mastocytosis with an associated clonal hematologic non-mast cell lineage disease (SM-AHNMD)... 

Bonadonna P, Perbellini O, Passalacqua G, et al Clonal mast cell disorders in patients with systemic reactions to Hymenoptera stings and increased serum tryptase levels. J Allergy Clin Immunol 2009 123 680-686. 

These are supplied by the secretion of peptide molecules (termed cytokines or lymphokines) fiom a subset of the T-cell family (the helper T cells, TH cells). These peptide molecules (interleukins (IL) 2,4,5 and 6) stimulate the B cells to proliferate, undergo clonal expansion and mature into plasma cells which secrete antibody and also into the longer-hving, non-dividing memory cells. 

Clonal deletion. Contact with antigen in the neonate results in death or permanent inactivation of the developing lymphocytes. 

Syrian hamster embryo cells (clonal assay) Cell transformation No data — Amacher and Zelljadt 1983... 

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