Tick-induced modulation of the host immune response.

The tick-host-pathogen interface is characterised by complex immunological interactions. Host immune responses to tick infestation and infection with tick-borne pathogens involve cytokines, antibodies, complement and T lymphocyte regulatory and effector pathways. A successful host-parasite relationship is a balance between limiting the parasite by host defenses and the ability of the parasite to modulate, evade or restrict the host response. Hosts acquire immunological based resistance to tick infestation, which reduces engorgement, production of ova and viability. Salivary glands of ixodid ticks produce a complex array of immunogens and pharmacologically active molecules. Tick salivary gland derived material can modulate host cytokine, antibody and cell mediated immune responses. Both immunoregulatory and immune effector pathways of the host are suppressed. Tick feeding impairs the ability to develop a primary immune response to a thymic dependent immunogen. Lymphocytes obtained from tick infested hosts are reduced in their ability to proliferate in vitro to T lymphocyte mitogens, while responses to B lymphocyte polyclonal activators are unaltered. Normal macrophages and lymphocytes were exposed to female tick salivary gland extracts prepared daily during the course of engorgement. All extracts reduced lymphocyte responses to T cell mitogens and enhanced in vitro proliferation in the presence of a B lymphocyte mitogen. Macrophage elaboration of tumour necrosis factor alpha and interleukin-1 are significantly reduced in a differential manner. Production of interleukin-2 and interferon-gamma by T lymphocytes is reduced. Tick modulation of the host immune response could enhance the ability of the arthropod to obtain a blood meal and facilitate pathogen transmission to an immunocompetent host.