Effector

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effector

[ə′fek·tər]
(biochemistry)
Anactivator of an allosteric enzyme.
(control systems)
A motor, solenoid, or hydraulic piston that turns commands to a teleoperator into specific manipulatory actions.
(physiology)
A structure that is sensitive to a stimulus and causes an organism or part of an organism to react to the stimulus, either positively or negatively.

Effector

 

(1) The terminal link in the chain of neurons in the reflex arc. The effectors of the central nervous system transmit impulses to the peripheral organs and tissues.

(2) In animals and man, one of the effector organs by means of which the body responds to external and internal stimuli or engages in work activity. Depending on the nature and purpose of the response, effectors form dynamic systems that include various organs; for example, in the case of physical labor they include the muscles, blood vessels, heart, and endocrine glands. Chromatophores, luminescent organs, and electric organs are also included in the category of effectors.

Effector regulation takes place both on the organ level and on the level of cellular and subcellular formations; such regulation performs the function of triggering the beginning and cessation of work and has an adaptotrophic effect (intensiveness and qualitative characteristics of the effector reaction). The composition and interrelation of the effectors within a system depend on the degree of conditioning and reinforcement of the response and on the state of the effectors.

(3) In biochemistry, a metabolic product that by combining with an enzyme increases or diminishes its activity.

V. I. MEDVEDEV

References in periodicals archive ?
PD-L1 is a negative immunomodulatory ligand expressing on cancer cells, which binds PD-1 on immune effector cells (such as T cell and NK cell) to reduce their immune effect function.
Here, several parameters remain to be defined given that there is a fine interplay between the scFv, spacer, transmembrane, signaling domains, and the effector cell type.
These in vitro data suggested that crosslinking through tumor target binding was required for Fc[gamma]R-mediated effector cell activation and is analogous to the ability of crosslinking through Fc[gamma]R engagement to promote signaling through TweakR as discussed above.
Treg cells inhibit the pro-inflammatory activity of macrophages, which are the major immune effector cells in TNF-mediated psoriasis.
Effector cells (E) target and destroy infected and noninfected tumor cells (T; and Tu) at a rate [p.sub.3] and take up BCG at a rate [p.sub.1].
Among other immune cells, NK and NKT cells, together with the M1, M2, M4, and M17 macrophages, form a network of cells and either respond immediately to the presence and entry of harmful agents or function as effector cells through their microbicidal mechanisms.
Recently, it has also been described that Tregs secrete microRNAs which could be implicated in inhibiting T effector cells, thus opening a new area of interest in Treg-mediated suppressive mechanisms [23].
Tregs are a natural part of the human immune system that regulate the activity of T effector cells, which are responsible for protecting the body from viruses and other foreign antigens.
The main cytokines of the adaptive immune response, the effector cells, and their principle actions are explained separately.
Naive ([CD45RA.sup.+] [CD62L.sup.+] or [CD45RA.sup.+] [CCR7.sup.+]), Tem ([CD45RA.sup.-] [CD62L.sup.-] or [CD45RA.sup.-] [CCR7.sup.- ]), and Tcm ([CD45RA.sup.-] [CD62L.sup.+] or [CD45RA.sup.-] [CCR7.sup.+]) cells were determined in both [CD4.sup.+] and [CD8.sup.+], whereas effector cells ([CD45RA.sup.+] [CD62L.sup.-] or [CD45RA.sup.+] [CCR7.sup.-]) were presented in only [CD8.sup.+].
These cells are potent effector cells and can produce cytokines such as IFN-[gamma], IL-4, IL-13, TNF-[alpha] [73, 74], and IL-10 [75].