Upon infection, our immune cells produce a small protein called interferon, which in turn signals a protective response through a series of biochemical reactions that involves lowering the cells' ability to make cholesterol by targeting a gene essential for controlling the pathway for cholesterol metabolism.

Transforming growth factor beta 1 (TGF-beta 1) has been shown to be associated with active centers of hematopoiesis and lymphopoiesis in the developing fetus. Therefore, the effects of TGF-beta 1 on mouse hematopoiesis were studied. TGF-beta 1 is a potent inhibitor of IL-3-induced bone marrow proliferation, but it does not inhibit the proliferation induced by granulocyte/macrophage, colony-stimulating factor (CSF), granulocyte CSF, and erythropoietin (Epo). TGF-beta 1 also inhibits IL-3-induced multipotential colony formation of bone marrow cells in soft agar, which includes early erythroid differentiation, while Epo-induced terminal differentiation is unaffected. In addition, IL-3-induced granulocyte/macrophage colonies were inhibited; however, small clusters of differentiated myeloid cells were consistently seen in cultures containing IL-3 and TGF-beta 1. Thus, TGF-beta 1 selectively inhibits early hematopoietic progenitor growth and differentiation but not more mature progenitors. TGF-beta 1 is also a potent inhibitor of IL-3-dependent and -independent myelomonocytic leukemic cell growth, while the more mature erythroid and macrophage leukemias are insensitive. Therefore, TGF-beta 1 functions as a selective regulator of differentiating normal hematopoietic cells, and suppresses myeloid leukemic cell growth.

It is concluded that HCC may be a malignancy worthy of DC trials and sufficient details in the present paper are given for the protocol to be copied or modified.

Activated macrophages play a central role in controlling inflammatory responses to infection and are tightly regulated to rapidly mount responses to infectious challenge. Type I interferon (alpha/beta interferon [IFN-␣/␤]) and type II interferon (IFN-␥Murine cytomegalovirus (MCMV) infection in mice is a well-established model system for the study of acute, persistent, and latent infections of betaherpesviruses and their control by the host immune system (32,35,58,60). Both human CMV (HCMV) and MCMV infect a broad range of tissues in their respective hosts, including fibroblasts, endothelial and epithelial cells, and, significantly, immune cells of the myeloid lineage (13,57,69,70). Differentiated macrophages of this lineage residing in infected tissues play a key role in eliciting the host immune response but are also permissive for CMV infection and serve as disseminators of the virus throughout the host (reviewed in reference 29).In immunocompetent hosts, primary CMV infections are generally asymptomatic, with immune cells either killing virusinfected cells or restricting viral cell-to-cell spread and replication. The latter effect occurs via induction of an antiviral state in noninfected cells or the activation of immune cells by soluble mediators such as type I interferon (alpha/beta interferon [IFN-␣/␤]) and type II interferon (IFN-␥) (8,10,41,50,60,73). Several hundred genes stimulated in response to both type I and type II IFNs have been identified by microarrays in various cell types over the years (18,19,37,38,66). In contrast, the recently discovered type III IFNs are not well characterized but may have comparable functions to the type I IFNs, mediated by shared downstream signaling and IFN-stimulated genes (ISGs) (3, 33, 42, 63, 72, 78, 84). Type III IFNs are