Influence of REV and ALV-J Co-Infection on Immunologic Function of T Lymphocytes and Histopathology in Broiler Chickens

The aim of present investigation is to study the effect of single- and co-infection with REV and ALV-J on T lymphocytes bioactivities and histopathology in broiler chickens. The bioactivities of blood and spleen T lymphocytes including lymphoproliferation responses, cytotoxicitic responses, and histopathology of spleen were detected in broiler chickens singly- or co-infected with REV and ALV-J at different days post inoculation and the virus expressions in spleen of infected broiler chickens were detected with immunofluorescence assay （IFA）. The results indicated that blood and spleen T lymphocytes proliferation responses and cytotoxicity in broilers infected with REV or/and ALV-J were inhibited in the whole observed period compared with controls. In the co-infected chickens they were highly inhibited than in the single-infected. The histopathology of spleen in infected chickens at 17 and 37 d post inoculation （dpi） indicated that cell interium increased, the numbers of lymphocytes decreased, and the regrowth were destroyed or decreased, especially more significantly at 17 than at 37 dpi. The different numbers of virus were detected in spleen lymphocytes in REV- infected and/or ALV-J-infected chickens. In the spleen of co-infected chicken, both REV and ALV-J were detected and the total numbers of viruses were more than in chickens singly-infected with REV or ALV-J. Thus, the co-effect of REV and ALV-J caused more immunosuppression on T lymphocytes bioactivities in broiler chickens than single-effect of ALV-J or REV, which contributed to the sever histopathology and the product of tumor cells. This study will be helpful for understanding the effect of co-infection with many viruses and control them in poultry.

Role of CD80 in stimulating T lymphocyte activation

AIM： To observe biological characteristics of hepatocarcinoma cells before and after CD80 transfection and to compare the effect of CD80-transfected hepatocarcinoma cells on T lymphocyte activation. METHODS： Retro virus vector carrying CD80 gene was transfected into HepG2 cells to establish CD80transfected hepatocarcinoma cells （HepG2/hCD80）. Flow cytometry （FCM） was performed to detect CD80 expression in the transfected cells. RT-PCR was used to evaluate CD80 expression at mRNA level. In the presence of anti-CD3 mAb, the proliferation of T lymphocyte was observed by M＇n＇. Meanwhile, the expression of activated molecule marker CD25 was analyzed through FCM. RESULTS： A stable cell line HepG2/hCD80 expressing the human CD80 was established. Growth curve showed that the molecule CD80 could obviously decrease the growth of tumor cells. HepG2/hCD80 was evidenced to have a potency to enhance T cell proliferation and upregulate CD25 expression. CONCLUSION： CD80 transfection can lower malignant phenotype of hepatocarcinoma cells. CD80 transfection has a down-regulatory effect to activated T cells in vitro.

THE IMMUNOREGULATORY EFFECT OF TLSF_(JM) ON THE EXPRESSION OF T CELL IL-2R AND PROTEIN TYROSINE PHOSPHORYLATION

The immunoregulatory effect of TLSFJM on the expression of T cell IL- 2R and protein tyrosine phosphorylation ( PTP ) was investigated by immunohistochemistry technique. The results showed that TLSFJMcan markedly suppress the expression of IL-2R and PTP on PHA or TPA-stimulated human PBMC and murine IL-2 dependent cell line CTLL-2. However, there was no effect of TLSFJMon the production of IL-1, IL-2 and IL-6 that play an important role in the course of T lymphocyte proliferation and differentiation.

Activated cytotoxic lymphocytes promote tumor progression by increasing the ability of 3LL tumor cells to mediate MDSC chemoattraction via Fas signaling

The Fas/FasL system transmits intracellular apoptotic signaling, inducing cell apoptosis. However, Fas signaling also exerts non-apoptotic functions in addition to inducing tumor cell apoptosis. For example, Fas signaling induces lung cancer tumor cells to produce prostaglandin E2 （PGE2） and recruit myeloid-derived suppressor cells （MDSCs）. Activated cytotoxic T lymphocytes （CTLs） induce and express high levels of FasL, but the effects of Fas activation initiated by FasL in CTLs on apoptosis-resistant tumor cells remain largely unclear. We purified activated CD8^＋ T cells from OT-1 mice, evaluated the regulatory effects of Fas activation on tumor cell escape and investigated the relevant mechanisms. We found that CTLs induced tumor cells to secrete PGE2 and increase tumor cell-mediated chemoattraction of MDSCs via Fas signaling, which was favorable to tumor growth. Our results indicate that CTLs may participate in the tumor immune evasion process. To the best of our knowledge, this is a novel mechanism by which CTLs play a role in tumor escape. Our findings implicate a strategy to enhance the antitumor immune response via reduction of negative immune responses to tumors promoted by CTLs through Fas signaling.