T cell proliferation

Anticytokine receptor antibodies Basiliximab, Da-cluzimab Both are humanized monoclonal antibodies against the IL-2 receptor that block T-cell proliferation by inhibiting IL-2 and thus decrease the T-cell mediated frequency of rejection episodes in organ transplantation. 

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. 

Migueles SA, Laborico AC, Shupert WL, Sabbaghian MS, Rabin R, Hallahan CW, Van Baade D, Kostense S, Miedema F, McLaughlin M, Ehler L, Metcalf J, Liu S, Connors M (2002) HIV-specific CD8+ T cell proliferation is coupled to perforin expression and is maintained in non-progressors, Nat Immunol 3 1061-1068... 

Restivo VA Jr, Lombard LA. Gray GS. Nadler LM Cloning of B7-2 a CTLA-4 counter-receptor that 79 costimulates human T cell proliferation. Science 1993 262 909-911. 

Fever is the most common manifestation. The thermoregulatory centre in the hypothalamus regulates body temperature and this can be affected by endotoxins (heat-stable lipopolysaccharides) of Gram-negative bacteria and also by a monokine secreted by monocytes and macrophages called interleukin-1 (IL-1) which is also termed endogenous pyrogen. Antibody production and T-cell proliferation have been shown to be enhanced at elevated body temperatures and thus are beneficial effects of fever. 

ATLURU s, ATLURU D (1991) Evidence that genistein, a protein-tyrosine kinase inhibitor, inhibits CD28 monoclonal antibody stimulated human T-cell proliferation. Transplantation. 51 448-50. 

The sterols and sterolins in rice bran are potent immunomodulators. The best response was obtained with a 100 1 sterol/sterolin mixture that demonstrated T-cell proliferation from 20% to 920% and active cell antigens after four weeks in human subjects (Bouic et al, 1996). Another in vitro experimental study with sterol/sterolins, demonstrated a significant increase in cytokinines, interleukin-2 and y-interferon between 17% and 41 % in addition to an increase in natural killer cell activity. These experiments (Bouic et al, 1996) prove that sterol/sterolins are potent immunomodulators with important implications for the treatment of immune dysfunction. Rice bran products are excellent dietary supplements for the improvement of immune function. It is probable that the effects of rice bran on diabetes, CVD and cancer all result from improved immune function. 

Whey proteins are known to increase immune response and maintain muscle mass (Phillips et ah, 2009). In one instance, when an immunosti-mulatory vitamin and mineral mixture developed at Tufts University Human Nutrition Research Center on Aging was blended with texturized WPI (TWPI) in an extruded snack bar, immunostimulatory effects were enhanced in young (< 5 months) and old (> 22 months) mice fed ad libitum for 5 weeks. The mineral mixture and TWPI improved T cell proliferation and reduced upregulated production of proinflammatory mediators in... 

The antiproliferatives azathioprine and the mycophenohc acid derivatives inhibit T cell proliferation. Myelosuppression is the most significant adverse event associated with these agents. 

Azathioprine was originally approved by the FDA in 1968 as an adjunct immunosuppressant for use in renal transplant recipients. It is available in oral and IV dosage forms.11 Prior to the advent of cyclosporine, the combination of azathioprine and corticosteroids was the mainstay of immunosuppressive therapy. Over the past 10 years, the use of azathioprine has declined markedly due in large part to the success of the MPA derivatives, which are more specific inhibitors of T cell proliferation. 

DL-10 (35) T cell, fibroblast Suppression of B- and T-cell proliferation. Inhibition of LPS-induced monocyte IL-1, IL-8, and TNF production. Induction of IL-lra. Suppression of free radical release and NO-dependent microbicidal activity of macrophages. 

Naisbitt, D.J., Fraser Gordon, S., Pirmohamed, M., Burkhart, C., Cribb, A.E., Pichler, W.J., and Kevin Park, B., Antigenicity and immunogenicity of sulphamethoxazole demonstration of metabolism-dependent haptenation and T-cell proliferation in vivo, Br. J. Pharmacol., 133, 295, 2001. 

FIGURE 7.4 (A) Donor CD4+T cell proliferation, as reflected by dilution of the fluorescence associated with CFSE, is not altered by TCDD exposure. Changes in expression ofT cell activation markers (B) CD62L and (C) CD25, are induced by TCDD exposure and are dependent on cell division. Data represent donor CD4+ T cells responding to alloantigen in F1 hosts 48 hours after adoptive transfer. F1 host mice were treated with vehicle or TCDD one day prior to injection of CFSE-labeled donorT cells. Adapted from Funatake et al., 2005. 

In vitro TGN1412 caused a profound, polyclonal T-cell proliferation of human peripheral blood mononuclear cells, including those from patients with BCLL. It also induced a profound activation and proliferation of T-cell subsets including CD4+ and CD8+ T cells, naive and memory T cells, and regulatory T cells. TGN1412 was shown to induce a transient, well tolerated expansion of T cells in nonhuman primates treated with TGN1412 and efficacy was demonstrated in a rhesus monkey collagen-induced arthritis model. 

Brunner, M.C. et al., CTLA-4-mediated inhibition of early events of T cell proliferation, J. Immunol., 162, 5813, 1999. 

One of the most sensitive alterations induced by Pb is the capacity to impair NO production by macrophages. Several groups have shown that exposure to Pb significantly reduces NO production [51,61,62], and this impaired NO production may be the basis of certain aspects of Pb immunotoxicity including reduced host resistance to Listeria [23] and increased T cell proliferation in response to allo-antigen [Farrer and McCabe, unpublished data]. 

Farrer, D. F., Hueber, S. and McCabe, Jr., M.J., Lead enhances CD4+ T cell proliferation indirectly by targeting antigen presenting cells and modulating antigen-specific interactions, Toxicol. Appl. Pharmacol. In Press, 2005. 

Disparate effects on T-cell proliferative responses have been reported following exposure to JP-8. Significant suppression of T-cell proliferation is reported following either inhalation or dermal exposure to JP-8 [ 18,20,36], while the response is unaffected following either the oral or dermal exposure routes in other studies [66,71,72], These differences may be explained by variations in exposure routes and in assay methodology, as agents used to evaluate T-lymphocyte activation and proliferation were diverse and included Con A plus IL-2 [18,20], anti-CD3 [36], or Con A only [66,71,72],... 

Cell-mediated immunity Mitogen-induced T-cell proliferation, NK cell activity Spontaneous cytotoxicity assays... 

Several cytokines have been characterized at the molecular level in different species of marine mammals (Table 23.2). In addition, limited evidence exists for conserved functionality of cytokines in marine mammals, such as the ability of human recombinant IL-2 to stimulate T cell proliferation [32, 33] and natural killer cell activity [39,40] in beluga whales and harbor seals. Assays were developed to quantify circulating levels of cytokines [41,42], as well as C-reactive protein, a marker of acute inflammation [43],... 

Mori, C. et al., Immunomodulatory effects of in vitro exposure to organochlorines on T cell proliferation in marine mammals and mice, J. Toxicol. Environ. Health, 69, 283, 2006. 

Tough, D.F., Borrow, R, and Sprent, J., Induction of bystander T cell proliferation by viruses and type I interferon in vivo, Science, 272, 1947, 1996. 

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