Analysis of B7-1 and B7-2 costimulatory ligands in cultured mouse microglia: upregulation by interferon-γ and lipopolysaccharide and downregulation by interleukin-10, prostaglandin E2 and cyclic AMP-elevating agents

Prostaglandin and the Suppression of Phagocyte Innate Immune Responses in Different Organs

“…In the CNS, PGE 2 primarily causes enhanced levels of cAMP [80], which further suggests a role for EP 2 and EP 4 in the mediation of CNS inflammation. Supporting its suppressive functions, studies of TLR4-mediated microglial activation have shown that PGE 2 can inhibit the production of TNF- α [86] and IL-12 [87], IL-18 [88], the expression of the B7-2 (CD86) co-stimulatory molecules [89], the enhancement of IL-10 and IL-6 production, and the expression of inducible nitric oxide synthase (iNOS). Additionally, a recent study has associated PGE 2 with decreased microbicidal activity by microglial cells in meningitis [90].…”

Toll-Like Receptors in Brain Abscess

“…The importance of microglia in the early host response to infection in brain abscess is suggested by the fact that pro-inflammatory mediator production is detected within 1 to 3 hours following the initial S. aureus infection, well before the significant accumulation of peripheral immune cell infiltrates (Kielian and Hickey 2000; Esen et al 2004). Moreover, both heat-inactivated S. aureus and PGN are capable of inducing microglial MHC Class II, CD40, CD80, and CD86 expression (Kielian 2002b; Kielian et al 2004a; Esen and Kielian 2007), similar to what has been described for microglia in response to the Gram-negative bacterial cell wall product lipopolysaccharide (LPS) and interferon-γ (IFN-γ) (Frei et al 1994; Xu and Ling 1995; Menendez Iglesias et al 1997; Aloisi 1998; O’Keefe et al 2001). The ability of S. aureus to augment the expression of receptors that are important for antigen presentation suggests that the ability of microglia to present bacterial peptides to antigen-specific T cells may be greatly enhanced following S. aureus exposure.…”

Immunomodulators in human seminal plasma: a vital protection for spermatozoa in the presence of infection?

“…PGE has been shown to induce anergy directly (Mannie et al, 1995) but could also induce it directly by stimulating IL-10 and inhibiting IL-12 (Table 2). Both PGE (Iglesias et al, 1997) and IL-10 (Ding et al, 1993;Willems et al, 1994;Chang et al, 1995) can down-regulate the co-stimulatory molecule B7 on antigen presenting cells and thus this is the likely mechanism for induction of anergy (Table 3).…”

“…One mechanism in formation of anergic T cells is the presentation of antigen in the absence of co-stimulatory signals such as B7.2 (CD86). CD86 is upregulated by interferon c and LPS and down regulated by IL-10 and PGE (but not by TGFb) (Iglesias et al, 1997). Because the effects of interferon c and bacterial components such as LPS are not speci®c to the cell presenting bacterial antigen, T cells presented with spermatozoal antigen in the presence of infection will also be primed and stimulated ± speci®cally against sperm antigen!…”