Induction of Target Cell Apoptosis by Channel Catfish Cytotoxic Cells

Fighting Virus and Parasites with Fish Cytotoxic Cells

“…This receptor showed important features: 1) the 5C6 antibody recognizes the NCCs of most studied fish and even the mammalian NK and LAK cells, demonstrating its conservation (Cuesta et al, 2005a;Evans et al, 1988;Jaso-Friedmann & Evans, 1999;McKinney & Schmale, 1997); 2) the NCC activity is blocked by the 5C6 antibody Iwanowicz et al, 2004;JasoFriedmann et al, 1988JasoFriedmann et al, , 2001; 3) the NCCRP-1 is a 32-34 kDa protein found in the membrane of NCCs and binds to a 42 and 46 kDa from the tumor targets and protozoan that they kill, respectively (Evans et al, 1996;Jaso-Friedmann et al, 1997a, 1997bLester et al, 1994); and 4) it is a type-III membrane protein and its activation led to tyrosine and serine phosphorylation and uses the Jak-STAT signalling pathway (Evans et al, 1999;JasoFriedmann et al, 1995JasoFriedmann et al, , 2001. After binding to the target cell, mammalian NKs and fish NCCs share the same killing mechanisms including granule-dependent (release of perforin and granzymes) and granule-independent (Fas/FasL system) (Cuesta et al, 2003a;Hogan et al, 1999;Jaso-Friedmann et al, 2000;Shen et al, 2002). The release of perforin and granzyme contained in the granules is calcium-dependent and the NCC activity is greatly inhibited or completely abrogated by Ca 2+ -chelators demonstrating their involvement in the NCCmediated cytotoxic activity (Carlson et al, 1985;Hogan et al, 1999).…”

“…After binding to the target cell, mammalian NKs and fish NCCs share the same killing mechanisms including granule-dependent (release of perforin and granzymes) and granule-independent (Fas/FasL system) (Cuesta et al, 2003a;Hogan et al, 1999;Jaso-Friedmann et al, 2000;Shen et al, 2002). The release of perforin and granzyme contained in the granules is calcium-dependent and the NCC activity is greatly inhibited or completely abrogated by Ca 2+ -chelators demonstrating their involvement in the NCCmediated cytotoxic activity (Carlson et al, 1985;Hogan et al, 1999). In the last decade, fish perforin (Athanasopoulou et al, 2009;Hwang et al, 2004;Toda et al, 2011a) and granzyme (Huang et al, 2010;Praveen et al, 2004Praveen et al, , 2006Wernersson et al, 2006) sequences have been obtained but their gene expression or function has been scarcely related to the innate cytotoxic activity (Ordás et al, 2011;Praveen et al, 2006).…”

“…In catfish peripheral blood leucocytes (PBL), two populations of NK-like cells have been identified: one able to kill allogeneic, but not autologous, cells and the other able to kill virus-infected catfish cells (Hogan et al, 1996(Hogan et al, , 1999Shen et al, 2002Shen et al, , 2004Stuge et al, 1997Stuge et al, , 2000Yoshida et al, 1995). These NK-like cells were able to proliferate after weak alloantigen stimulation and presence of specific growth factors giving to clonal NK-like cells, what has greatly allowed further characterization.…”

“…Clonal catfish NK cells induced apoptosis in their target cells by means of the calcium-dependent perforin/granzyme-mediated secretory lytic pathway since Ca-chelators completely abolished their cytotoxic activity (Hogan et al, 1999). Moreover, an antibody against leucocyte-function-associated antigen (LFA)-1, which is an adhesion molecule, inhibited the clonal catfish NK-like cell activity (Yoshida et al, 1995).…”

“…Fish NCC activity has been shown to be modulated by several chemicals, cytokines, environmental contaminants, stress factors, immunostimulants, etc. First studies dealt with the NCC inhibition by blocking the binding to target in order to characterize the role of NCCRP-1, or inhibiting the killing mechanisms in order to evaluate the perforin-or Fas/FasL-mediated lytic pathway (Bishop et al, 2002;Carlson et al, 1985;Evans et al, 1988Hogan et al, 1999;Iwanowicz et al, 2004;Jaso-Friedmann et al, 1988Kaur et al, 2004;Shen et al, 2002). Further studies demonstrated that catfish NCC activity is increased by leucocyte treatment with ionophore A23187, A23187 plus phorbol myristate acetate (PMA) or vanadate but no with PMA alone or poly I:C (a mimic for viral infections) (Evans et al, 1984b(Evans et al, , 1990(Evans et al, , 1998b.…”