Premium
Mechanism of up‐regulation of immunoglobulin A production in the intestine of mice unresponsive to lipopolysaccharide
Author(s) -
Kaneko Masahiro,
Akiyama Yoshiyuki,
Takimoto Hiroaki,
Kumazawa Yoshio
Publication year - 2005
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2005.02198.x
Subject(s) - biology , lipopolysaccharide , tlr4 , spleen , small intestine , lamina propria , immunology , cholera toxin , immune system , antibody , cytokine , transforming growth factor , microbiology and biotechnology , endocrinology , epithelium , genetics
Summary The mechanisms by which immunoglobulin A (IgA) production up‐regulates in the intestine of Toll‐like receptor‐4 (TLR4)‐mutated mice were investigated. When TLR4‐mutated, C3H/HeJ and BALB/lps d mice received oral administration of cholera toxin (CT), not only CT‐specific IgA levels in the intestinal lavage but also the number of IgA‐producing cells in intestinal lamina propria (iLP) significantly increased compared with those of the wild‐type C3H/He and BALB/c mice. Interleukin (IL)‐5‐producing cells and CD86 + cells in iLP also significantly increased in C3H/HeJ mice. The expression of major histocompatibility complex class II and CD86 on cells present in Peyer's patches (PPs) of C3H/HeJ mice was higher than those of C3H/He mice. In non‐immunized C3H/HeJ mice, the expression of transforming growth factor‐β (TGF‐β) mRNA and the percentages of IL‐10‐producing cells in PPs but not in spleen increased when compared with those in C3H/He mice. The suppressor of cytokine signalling‐1 (SOCS‐1) was expressed in PPs of C3H/He mice but not C3H/HeJ mice. These results indicate that high IgA levels in the intestine of TLR4‐mutated mice are due to up‐regulation of TGF‐β and IL‐10 and the lack of regulation by SOCS‐1.