Specific cell-mediated cytotoxicity

Cells involved in non-specific cell-mediated cytotoxicity (CMC)... 

NCC and NK-like cells have been reported to be involved in non-specific cell-mediated cytotoxicity (CMC) in fish. NCCs were originally described in channel catfish and are the most extensively studied killer cell population in teleosts. NCCs spontaneously kill a wide variety of target cells including tumour cells, virally transformed cells and protozoan parasites, and express components of the granule exocytosis pathway of CMC similar to mammalian cytotoxic lymphocytes (Froystad et al., 1998 Praveen et al., 2004). Catfish NCCs are small agranular lymphocytes that express a novel type III membrane protein termed the NCC receptor protein 1 (NCCRP-1) (Evans et al., 1984). NCC activity has been described in other fish species including rainbow trout, carp, damselfish and tilapia (Shen et al., 2002). 

Expression profiles of TCRbeta and CD8alpha mRNA correlate with virus-specific cell-mediated cytotoxic activity in ginbuna crucian carp . Virology, 348, 370-7. 

Null cells Antihody-dependent cell-mediated cytotoxicity (ADCC) involving non-T/non-B cells (null cells) with Fc receptors specific for antihody-coated target cells. 

Another effector function is the cell-mediated cytotoxicity. Infected cells that were recognized and opsonized by specific antibodies can be lysed by natural killer cells which are the classical K cells. These properties are highly determined by the Fc part of antibodies. IgGl and IgG3 have the highest capacity for cell-mediated cytotoxicity. The effector function of an antibody is frequently used as a mean of antibody recognition. This is especially the case with bacterial proteins such as protein A and protein G that specifically interact with the same domain. Therefore purification can interfere with the antibody effector function. 

Hyperacute rejection may occur when preformed donor-specific antibodies are present in the recipient at the time of the transplant and may be evident within minutes of the transplant procedure. Hyperacute rejection can be induced by immunoglobulin G (IgG) antibodies that bind to antigens on the vascular endothelium, such as class I MHC, ABO, and vascular endothelial cell antigens. Tissue damage can be mediated through antibody-dependent, cell-mediated cytotoxicity or through activation of the complement cascade. The ischemic damage to the microvasculature rapidly produces tissue necrosis. 

In recent years, interest has focused on the role of cell-mediated immune response in melanoma. Specific cell-mediated responses may play a role in tumor regression, but the role of specific cells such as cytotoxic T lymphocytes (CTLs) is not fully understood. Tumor-infiltrating lymphocytes (TILs) have been shown in vivo and in vitro to possess antitumor reactivity. TILs contain a large number of mature tumor-specific lymphocytes and have been a target for manipulation in immunotherapeutic approaches for melanoma. 

Infliximab was designed specihcally to target TNF-a. It also may have more complex actions. Etaneracept, another anti-TNF-a therapy that uses a circulating receptor to clear soluble TNF-a, blocks its biologic effects but is ineffective in Crohn s disease. Infliximab binds membrane-bound TNF-a and may cause lysis of these cells by anti-body-dependent or cell-mediated cytotoxicity. Thus, infliximab may deplete specific populations of subepithelial inflammatory cells. These effects, together with its mean terminal plasma half-life of 8 to 10 days, may explain the prolonged clinical effects of infliximab. 

Both bryostatin 1 and 12-0-tetradecanoylphor-bol-13-acetate inhibited lymphocyte antibody-dependent cell-mediated cytotoxicity such that, at a 20 1 effector-to-target ratio, control lymphocytes had a mean 49 12% specific Cr release of antibody-coated target cells while bryostatin 1 and 12-O-tetradecanoylphorbol-13-acetate cultured lymphocytes had 12 6 and 8 12%, respectively, in four experiments (Tilden and Kraft 1991). 

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