Adaptive immunity has often been considered the penultimate of immune capacities. That system is now being deconstructed to encompass less stringent rules that govern its initiation, actual effector activity, and ambivalent results. Expanding the repertoire of innate immunity found in all invertebrates has greatly facilitated the relaxation of convictions concerning what actually constitutes innate and adaptive immunity. Two animal models, incidentally not on the line of chordate evolution (C. elegans and Drosophila), have contributed enormously to defining homology. The characteristics of specificity and memory and whether the antigen is pathogenic or nonpathogenic reveal considerable information on homology, thus deconstructing the more fundamentalist view. Senescence, cancer, and immunosuppression often associated with mammals that possess both innate and adaptive immunity also exist in invertebrates that only possess innate immunity. Strict definitions become blurred casting skepticism on the utility of creating rigid definitions of what innate and adaptive immunity are without considering overlaps.

ABSTRACT. We have demonstrated the presence of natural cytotoxic cells (NCC) against the murine cell line YAC-1 in tilapia (Tilapia mossambica X T honorum) fish. NCC-activities were observed in the anterior ludney, trunk kidney, spleen and peripheral blood. The highest cytotoxicity was found in the anterior kidney while the lowest was in the blood. Macrophages form over 70 % of conjugate forming cells (CFC) in anterior and trunk kidney as well as spleen, while lymphocytes represent the main CFC in peripheral blood. The optimum temperature for NCC activity was 28°C. Maximum S'Chromium release from labelled targets was between 3 and 6 h of incubation with anterior kidney leucocytes at 2E°C. We also have evidence for the production of cytotoxic factors(s) upon coincubation with YAC-1 cells. NCC diminishes as the fish mature and age.

Increasing ultraviolet-B irradiation (UVB) resulting from diminution of stratospheric ozone is becoming a serious international problem. UVB irradiation exerts not only carcinogenic effects on animals but also causes them to become vulnerable to infections by modulating their immune responses. UVB irradiation suppresses innate immune functions of cells such as macrophages, neutrophiIs, Langerhans cells, dendritic cells, and the serum component, complement. UVB irradiation also causes changes in cytokine profiles, represented by the induction of a paradigm switch involving Thl/Th2 phenotypes. According to earlier studies, Thl responses are suppressed, whereas Th2 activities are augmented by UVB irradiation. These immune modulations are caused by several pathways via cytokines and neuropeptides, and eventually may lead to increasing incidences of infection, allergy, and cancer. We have reviewed reports concerning UVB-irradiation induced immune modulation from the viewpoint of risks for human diseases and, in addition, for ecosystems and immunity of lower animals.

No abstract

No abstract