In alloimmunity, the body creates antibodies (called alloantibodies) against the alloantigens, attacking transfused blood, allotransplanted tissue, and even the fetus in some cases.
In case of hyperacute rejection, antibodies activate complement; moreover, the reaction can be enhanced by neutrophils.
Humoral (antibody-mediated) type of rejection is caused by recipient's B-lymphocytes which produce alloantibodies against donor MHC class I and II molecules.
Alternatively, donor cells are coated with alloantibodies that initiate phagocytosis through Fc receptors of mononuclear leukocytes.
[6] Cytokine microenvironment where CD4+ T-lymphocytes recognize alloantigens significantly influences polarization of the immune response.
It depends on the balance of activating and inhibitory NK cell receptors and on their ligands expressed by the graft.
If the graft has these ligands on its surface, NK cell cannot be activated (KIR receptors provide inhibitory signal).
It recognizes target cells by "missing-self strategy" [9] and induces their apoptosis by enzymes perforin and granzymes released from its cytotoxic granules.
This promotes APC maturation [10] which leads to amplification of T-cell alloreactivity by means of direct and also indirect pathway of alloantigen recognition (as described below).
NK cells are able to kill Foxp3+ regulatory T-lymphocytes as well [9] and shift the immune response from graft tolerance toward its rejection.
[12] However it is important to note that NK cell sub-populations differ in alloreactivity rate and in their immunomodulatory potential.
Transplanted tissue is accepted by immunocompetent recipient if it is functional in the absence of immunosuppressive drugs and without histologic signs of rejection.