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ABSTRACTThe immunoglobulin G (IgG) antibody is important for detecting and evaluating immune responses. Despite increasing opportunities for tigers to be exposed to emerging diseases due to global changes coupled with increasing interaction with humans, there is no available antibody specific to tigers. Aims of this study were to produce a rabbit anti-Bengal tiger (Panthera tigris tigris) IgG polyclonal antibody and to determine its specificity. The molecular weight of the purified Bengal tiger IgG was approximately 170 kDa. The cross-reactivity of rabbit anti-Bengal tiger IgG to IgG of other wild felid species and other domestic animals was analyzed by indirect enzyme-linked immunosorbent assay. The cross reactivity to other related wild animals ranged from 53.69% to 75.63%. There was high cross-reactivity with domestic cats (63.58%) and pigs (38.45%) and low cross-reactivity with domestic cows (10.46%), goats (8.60%), sheep (7.25%), and chickens (6.91%). To confirm cross-reactivity with domestic animals’ IgG, western blotting was performed. These results indicated that the purified rabbit anti-Bengal tiger IgG polyclonal antibody strongly reacted with species in the family Felidae. The polyclonal antibody generated in this study has the potential to aid in the development of useful tools for further novel immunological investigations on tigers and related felid species.

We performed a placebo-controlled study to evaluate the effects of immunomodulatory treatment with thalidomide on HIV levels, TNF-alpha levels, and immune status of 31 HIV-infected individuals, after temporary suppression of viral replication with antiretroviral drugs. Treatment with a combination of zidovudine and lamivudine (ZDV/LMV) for 14 days resulted in a median decline in plasma viremia of 1.94 log10 RNA equivalents/ml. After discontinuation of ZDV/LMV, thalidomide therapy (200 mg/day for 4 weeks) did not retard the prompt return of HIV titers to the pretreatment levels, and had no effect on plasma levels of TNF-alpha. In contrast, thalidomide treatment resulted in significant immune stimulation. We observed increased levels of plasma soluble IL-2 receptor, soluble CD8 antigen, and IL-12 (p < 0.01 for all parameters), as well as increased cutaneous delayed-type hypersensitivity reactions to recall antigens (p < 0.01) in thalidomide-treated patients. These changes were associated with a median increase in HIV titer of 0.2 log10 RNA equivalents/ml in the thalidomide-treated group (p < 0.05), which resolved after stopping the drug. Further studies were performed in vitro to elucidate the mechanism of thalidomide-induced immune stimulation. When purified T cells from HIV-infected individuals were stimulated by immobilized anti-CD3 in the presence of thalidomide, a costimulatory effect of the drug was observed, resulting in increased production of IL-2 and IFN-gamma, and increased T cell-proliferative responses. Further experiments showed that thalidomide increased IL-12 production by antigen-presenting cells in a T cell-dependent manner. Our findings suggest a potential application for thalidomide as a novel immune adjuvant in HIV disease.