Human T-cell leukemia virus type I and adult T-cell leukemia

Human T-Cell Lymphotropic Virus (HTLV-1) and Adult T-Cell Leukemia

“…In either route, HTLV-1-infected cells are essential for transmission. This was supported by the findings that fresh frozen plasma from carriers did not cause transmission and freezethawing of breast milk reduced vertical transmission (Matsuoka 2005). Transplacental transmission is also suspected.…”

“…A subtraction strategy between ATL cell lines and activated T cells identified I-309 as a secreted chemokine from ATL cells, and I-309 expression was remarkably enhanced in ATL cell lines. I-309 showed anti apoptotic effect v i a i t s r e c e p t o r C C R 8 , i n v o k i n g t h a t a n autocrine mechanism via I-309/CCR8 allowed ATL cells to survive in vivo (Matsuoka 2003). (Matsuoka 2005).…”

“…Thus, OX40 is also implicated in the cell adhesion and infiltration of ATL cells. Thus, ATL cells express various molecules that can modify their phenotypic properties, thereby modifying the clinical disease manifestation, and facilitating the survival of ATL cells (Matsuoka 2003). Hypercalcemia is frequently complicated in patients with acute ATL (more than 70% during the whole clinical course) (Kiyokawa et al 1987).…”

“…FOXP3 gene transcription can be detected in some ATL cases (10/17; 59%). Such ATL cells are thought to suppress the immune response via expression of immunoregulatory molecules on their surfaces, and production of immunosuppressive cytokines (Matsuoka 2005).…”

“…In addition to transcriptional changes, Tax is also well known to interact with cellular proteins and impair or alter their functions. For example, proteomic analyses of Tax-associated complexes showed that Tax could interact with cellular proteins, including the active forms of small GTPases, such as Cdc42, RhoA and Rac1, which should be implicated in the migration, invasion and adhesion of T-cells, as well as in the activation of the Jun-kinase (JNK) pathway (figure 3) (Matsuoka 2005). Tax1 upregulates the expression of genes encoding cytokines, chemokines, cell surface ligands, and their receptors, in an NF-κB, AP-1, CREB/ATF and/or NFAT dependent manner.…”