IL-10 Mediates Sigma1 Receptor-Dependent Suppression of Antitumor Immunity | Zendy

Li Zhu | Zendy; Sherven Sharma | Zendy; Brian Gardner | Zendy; Brian Escuadro | Zendy; Kimberly Atianzar | Zendy; Donald P. Tashkin | Zendy; Steven M. Dubinett | Zendy

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IL-10 Mediates Sigma1 Receptor-Dependent Suppression of Antitumor Immunity

Author(s) -

Li Zhu,

Sherven Sharma,

Brian Gardner,

Brian Escuadro,

Kimberly Atianzar,

Donald P. Tashkin,

Steven M. Dubinett

Publication year - 2003

Publication title -

the journal of immunology

Language(s) - Uncategorized

Resource type - Journals

SCImago Journal Rank - 2.737

H-Index - 372

eISSN - 1550-6606

pISSN - 0022-1767

DOI - 10.4049/jimmunol.170.7.3585

Subject(s) - receptor , sigma 1 receptor , splenocyte , pertussis toxin , immune system , in vivo , sigma receptor , biology , pharmacology , chemistry , agonist , cancer research , immunology , g protein , biochemistry , microbiology and biotechnology

Sigma receptors are unique endoplasmic reticulum proteins that mediate signaling for a variety of drugs. We determined the effect of sigma(1) receptor agonists on immune responses in a syngeneic lung cancer model. Sigma(1) receptor agonists, including cocaine, up-regulated splenocyte IL-10 mRNA and protein production in vitro in a sigma receptor-dependent, pertussis toxin-sensitive manner. In vivo, sigma(1) receptor agonists promoted tumor growth and induced IL-10 at the tumor site. Increased tumor growth was prevented by administration of specific Abs to IL-10 or by administration of specific sigma(1) receptor antagonists. We report that sigma(1) receptor ligands, including cocaine, augment tumor growth through an IL-10 dependent mechanism.

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