Words similar to effector
Example sentences for: effector
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The tiny RNAs associate with various silencing effector complexes and attach to homologous target sequences (RNA or DNA) by basepairing.
COX-2 is an inducible enzyme upregulated in inflammatory states [ 20 21 ] . Notably, many NSCLC and what have been characterized as "premalignant" lung lesions have been shown to constitutively express the COX-2 enzyme and produce prostaglandin E-2 (PGE-2), the primary product of the COX-2 pathway [ 22 23 24 25 26 ] . Importantly, PGE-2 production by tumor cells has been linked to tumor-induced immunosuppression in NSCLC [ 2 3 4 5 ] . PGE-2 has been shown to directly suppress T cell mediated immunity, the primary effector against tumor cells, at a variety of levels [ 2 3 4 5 6 7 ] . Further, PGE-2 has been shown to induce the IL10 in mononuclear cells [ 4 5 ] . IL10 is a prominent immunosuppressive cytokine that may have a dominant role in preventing innate antitumor responses in the NSCLC environment [ 2 3 4 5 ] , [ 8 9 10 11 12 13 14 15 16 17 18 19 ] . Among myriad suppressive effects on T cells and antigen presenting cells, IL10 is known to inhibit IL12 production [ 14 15 16 17 18 ] . IL12 plays a key role in the initiation and potentiation of cellular immune responses and alteration of the IL12 producing function in circulating mononuclear phagocytes may be a critical factor in suppressed T cell immunity to NSCLC [ 27 28 ] .
It has been recently appreciated that sufficient concentrations of secreted IFNg may also induce susceptible tumors to express the MHCII molecules, potentially leading to increased direct contact with CD4+ T cells [ 3 ] . Even though some reports indicate that tumor sensitivity to IFNg is not required to elicit tumor regression [ 4 ] , it is conceivable that the IFNg-induced MHCII expression on tumor cells may boost the effector phase of antitumor responses through additional cytokine release or direct tumor eradication by CD4+ T cells.
Under the same conditions, levels of total ERK1/2 (panel B), eIF4E (panel C), a downstream effector of ERK1/ERK2, and actin (panel E) showed no substantial change at all time points assayed, in control cells.
One mechanism could be through the selective recruitment of IFN-γ-producing effector cells.
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