Bovine IFNG ELISA Kit

The establishment of pregnancy is a complex process that requires a well-coordinated interaction between the implanting conceptus and the maternal uterus. In pigs, the conceptus undergoes dramatic morphological and functional changes at the time of implantation and introduces various factors, including estrogens and cytokines, interleukin-1 beta 2 (IL1B2), interferon-gamma (IFNG), and IFN-delta (IFND), into the uterine lumen. In response to ovarian steroid hormones and conceptus-derived factors, the uterine endometrium becomes receptive to the implanting conceptus by changing its expression of cell adhesion molecules, secretory activity, and immune response. Conceptus-derived estrogens act as a signal for maternal recognition of pregnancy by changing the direction of prostaglandin (PG) F-2a from the uterine vasculature to the uterine lumen. Estrogens also induce the expression of many endometrial genes, including genes related to growth factors, the synthesis and transport of PGs, and immunity. IL1B2, a pro-inflammatory cytokine, is produced by the elongating conceptus. The direct effect of IL1B2 on endometrial function is not fully understood. IL1B activates the expression of endometrial genes, including the genes involved in IL1B signaling and PG synthesis and transport. In addition, estrogen or IL1B stimulates endometrial expression of IFN signaling molecules, suggesting that estrogen and IL1B act cooperatively in priming the endometrial function of conceptus-produced IFNG and IFND that, in turn, modulate endometrial immune response during early pregnancy. This review addresses information about maternal-conceptus interactions with respect to endometrial gene expression in response to conceptus-derived factors, focusing on the roles of estrogen and IL1B during early pregnancy in pigs.

Interferon-gamma (IFNG) is a pleiotropic cytokine that modulates both innate and adaptive immune networks; it is the most potent activator of macrophages and a signature cytokine of activated T lymphocytes. Though IFNG is now appreciated to have a multitude of roles in immune modulation and broad-spectrum pathogen defense, it was originally discovered, and named, as a secretory factor that interferes with viral replication. In contrast to the prototypical type I interferons produced by any cells upon viral infection, only specific subsets of immune cells can produce IFNG upon infection or stimulation with antigen or mitogen. Still, virtually all cells can respond to both types of interferons. This makes IFNG a versatile anti-microbial cytokine and also gives it a unique position in the antiviral defense system. The goal of this review is to highlight the direct antiviral mechanisms of IFNG, thereby clarifying its antiviral function in the effective control of viral infections.