Tumor T-cell

TNF-P T cells Tumor cells, neutrophils, macrophages Cytotoxicity, phagocytosis... 

This is a single-chain receptor, which is a heavily glycosylated protein of 64kDa, associated with the IL-2R y-chain. Both membrane-bound and soluble forms of the IL-9R exist. It is expressed on T helper clones, macrophages, some T-cell tumors, and mast cell lines. ... 

IL-9 can support cell proliferation in the absence of an antigen or APC, Overproduction of it may lead to T-cell tumors, particularly of Th2 lymphocytes. In certain lymphomas, such as Hodgkin s lymphoma, it may act as an autocrine signal for cellular proliferation. IL-9 may play a role in the development of acute myeloblastic leukemia by stimulating leukemic cells to enter the S-phase rather than preventing cell death. In addition, IL-9 acts synergisticaUy with stem cell factor for recruitmg quiescent leukemic cells in the cell cycle. ... 

Finally, most commonly found in human T cell tumors is an inversion of chromosome 14 or a translocation of parts of the long arm of chromosome 14 to an-... 

The molecular identification of a plethora of T-cell tumor antigens that can serve as targets for many human cancers,... 

Tumor-associated antigen OVA Antigen presentation to CD4 T-cells, tumor regression in mice Tat 17... 

Gx to S phase cell-cycle transition. Transition is required for the onset of IL-2 induced T-cell proliferation. Additionally, SRL also attenuates growth factor induced proliferation of several nonimmune cells and also inhibits metastatic tumor growth and angiogenesis. 

Large granular lymphocytes, not belonging to either the T- or B-cell lineage. Natural killer (NK) cells are considered part of the innate defense system since, in contrast to cytotoxic T-cells, they are able to kill certain tumor cells in vitro without prior sensitization. The basal activity of NIC cells increases dramatically following stimulation with type I IFNs. In addition, NK cells display Fc-receptors for IgG and are important mediators of Antibody-Dependent-Cell-mediated-Cytotoxicity (ADCC). 

Retroviruses Human T-cell leukemia virus (HTLV) Human T-lymphocytic tumors... 

Booth V Keizer DW, Kamphuis MB et al (2002) The CXCR3 binding chemokine IP-IO/CXCLIO structure and receptor interactions. Biochemistry 41 10418-10425 Burns JM, Summers BC, Wang Y et al (2006) A novel chemokine receptor for SDF-1 and I-TAC involved in cell survival, cell adhesion, and tumor development. J Exp Med 203 2201-2213 Callebaut C, Krust B, Jacotot E et al (1993) T cell activation antigen, CD26, as a cofactor for entry of HIV in CD4+ cells. Science 262 2045-2050... 

CCR4-expresssing regulatory T cells is also stimulated via glioma cell secretion of CCL2. This may be an important mechanism whereby gliomas suppress anti-tumor immune responses and evade immune detection (Jordan et al. 2008). 

The inflammatory response in UC is propagated by atypical type 2 helper T cells that produce proinflammatory cytokines such as interleukin-1 (IL-1), IL-6, and tumor necrosis factor (TNF).7 As discussed previously, a genetic predisposition to UC may partially explain the development of excessive colonic and rectal inflammation. The finding of positive perinuclear antineutrophil cytoplasmic antibodies (pANCA) in association with the human leukocyte antigen (HLA)-DR2 allele in a large percentage of patients with UC supports this theory.4,12... 

Activated T cells begin releasing cytokines including interleukin-2 (IL-2), interferon-y, (IFN-y), tumor necrosis factor (TNF-a), and others.4,13 Cytokine activity leads to a rapid proliferation and turnover of skin cells, triggering the inflammatory process and the development of psoriatic skin lesions.4,13,14 TNF-a may have a role in disease severity it upregulates endothelial and keratinocyte expression of ICAM-1,... 

Probert L, Keffer J, Corbella P, et al. Wasting, ischemia, and lymphoid abnormalities in mice expressing T cell-targeted human tumor necrosis factor transgenes. J Immunol 1993 151(4) 1894—1906. 

Interleukin-6 (IL-6) is a small polypeptide with a molecular mass of 26 kDa (see Table 2). IL-6 can be induced in various cell types, including fibroblasts, macrophages/monocytes, epithelial cells, T cells, B cells, and diverse tumor cells (L4). TNF, IL-1, and LPS can stimulate IL-6 gene expression in macrophages/monocytes and fibroblasts. In vivo studies showed that systemic administration of TNF, LPS, and IL-1 was followed by a rapid induction of circulating IL-6 (B49, J2). Also, endothelin (ET) at concentrations observed pathophysiolog-ically may trigger production of IL-6 (Ml7). 

Cope, A.P., Liblau, R.S., Yang, X.D., Congia, M., Laudanna, C., Schreiber, R.D., Probert, L., Kollias, G. and McDevitt, H.O. (1997) Chronic tumor necrosis factor alters T cell responses by attenuating T cell receptor signaling. Journal of Experimental Medicine 185, 1573-1584. 

Corazza, N., Eichenberger, S., Eugster, H.P. and Mueller, C. (1999) Nonlymphocyte-derived tumor necrosis factor is required for induction of colitis in recombination activating gene (RAG)2( / ) mice upon transfer of CD4(+)CD45RB(hl) T cells. Journal of Experimental Medicine 190,1479-1492. 

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