The gammac cytokines play an important role in proliferation and survival of T cells. Blocking the gammac signals can cause the activated donor-reactive T cells losing the ability to proliferate, and getting into apoptosis pathway, which contributes to induction of the peripheral tolerance. In this study, we induced the transplant tolerance through blocking the gammac in combination with donor-specific transfusion (DST) in the cardiac transplantation. Following DST, on the day 2, 4 and 6, C57BL/6 recipients received anti-gammac monoclonal antibodies (mAbs) injection, and those in control group were not given anti-gammac mAbs. On the day 7, Balb/c cardiac allografts were transplanted. All recipients in experimental group accepted cardiac allografts over 30 days, and two of them accepted allografts without rejection until sacrifice on the 120 day. Animals only receiving DST rejected grafts within 5 days, and the mice receiving cardiac transplantation alone rejected grafts within 9 days. Our study showed that blockade of gammac signaling combined with DST significantly prolonged allograft survival, which was probably associated with inhibition of antigen-specific T-cell proliferation and induction of apoptosis.

To identify acute renal allograft rejection biomarkers in human serum, two-dimensional differential in-gel electrophoresis (2-D DIGE) and reversed phase high-performance liquid chromatography (RP-HPLC) followed by electrospray ionization mass spectrometry (ESI-MS) were used. Serum samples from renal allograft patients and normal volunteers were divided into three groups: acute rejection (AR), stable renal function (SRF) and normal volunteer (N). Serum samples were firstly processed using Multiple Affinity Removal Column to selectively remove the highest abundance proteins. Differentially expressed proteins were analyzed using 2-D DIGE. These differential protein spots were excised, digested by trypsin, and identified by RP-HPLC-ESI/MS. Twenty-two differentially expressed proteins were identified in serum from AR group. These proteins included complement C9 precursor, apolipoprotein A-IV precursor, vitamin D-binding protein precursor, beta-2-glycoprotein 1 precursor, etc. Vitamin D-binding protein, one of these proteins, was confirmed by ELISA in the independent set of serum samples. In conclusion, the differentially expressed proteins as serum biomarker candidates may provide the basis of acute rejection noninvasive diagnosis. Confirmed vitamin D-binding protein may be one of serum biomarkers of acute rejection. Furthermore, it may provide great insights into understanding the mechanisms and potential treatment strategy of acute rejection.

The γc cytokines play an important role in proliferation and survival of T cells. Blocking the γc signals can cause the activated donor-reactive T cells losing the ability to proliferate, and getting into apoptosis pathway, which contributes to induction of the peripheral tolerance. In this study, we induced the transplant tolerance through blocking the γc in combination with donor-specific trans-fusion (DST) in the cardiac transplantation. Following DST, on the day 2, 4 and 6, C57BL/6 recipients received anti-γc monoclonal antibodies (mAbs) injection, and those in control group were not given anti-γc mAbs. On the day 7, Balb/c cardiac allografts were transplanted. All recipients in experimental group accepted cardiac allografis over 30 days, and two of them accepted allografis without rejection until sacrifice on the 120 day. Animals only receiving DST rejected gratis within 5 days, and the mice receiving cardiac transplantation alone rejected gratis within 9 days. Our study showed that blockade of γc signaling combined with DST significantly prolonged allografi survival, which was probably associated with inhibition of antigen-specific T-cell proliferation and induction of apoptosis.

To identify acute renal allograft rejection biomarkers in human serum, two-dimensional differential in-gel electrophoresis (2-D DIGE) and reversed phase high-performance liquid chromatog-raphy (RP-HPLC) followed by electrospray ionization mass spectrometry (ESI-MS) were used. Serum samples from renal allograft patients and normal volunteers were divided into three groups: acute rejec-tion (AR), stable renal function (SRF) and normal volunteer (N). Serum samples were firstly processed using Multiple Affinity Removal Column to selectively remove the highest abundance proteins. Differ-entially expressed proteins were analyzed using 2-D DIGE. These differential protein spots were ex-cised, digested by trypsin, and identified by RP-HPLC-ESI/MS. Twenty-two differentially expressed proteins were identified in serum from AR group. These proteins included complement C9 precursor,apolipoprotein A-Ⅳ precursor, vitamin D-binding protein precursor, beta-2-glycoprotein 1 precursor,etc. Vitamin D-binding protein, one of these proteins, was confirmed by ELISA in the independent set of serum samples. In conclusion, the differentially expressed proteins as serum biomarker candidates may provide the basis of acute rejection noninvasive diagnosis. Confirmed vitamin D-binding protein may be one of serum biomarkers of acute rejection. Furthermore, it may provide great insights into un-derstanding the mechanisms and potential treatment strategy of acute rejection.

OBJECTIVETo analyze survival time of AIDS death cases receiving Antiretroviral Therapy and related factors.

METHODSA retrospective cohort study was carried out to collect the data on death cases receiving Antiretroviral Therapy by the National HIV/AIDS Comprehensive Response Information Management System. Kaplan-Meier was used to calculate the median survival time, and compare survival time among different groups of age, sex, marriage status, infectious routes, WHO clinical stage, baseline CD4(+)T cell counts, and interval time from the start of ART to HIV confirmation. Life table and survival curve were applied to describe survival distribution. Cox proportional hazard model was used to determine the factors associated with the survival time.

RESULTSAmong 142 AIDS death cases, 125 (88.03%) were related with AIDS and 17(11.97%) were not. The total median survival time was 3.100 months (95%CI: 2.279-3.921). The cumulative survival rate was (52 ± 4)%, (33 ± 4)%, (26 ± 4)% in the first 3 months, 3-6 months, and 6-12 months. The median survival time of married or cohabitation group was 2.670 months (95%CI:1.470-3.870), and single (unmarried, divorced, separation, widowed) group was 5.870 months (95%CI: 2.617-9.123). The median survival time of WHO clinical stage I or II group was 5.870 months (95%CI: 3.989-7.751), and WHO clinical stage III or IV group was 1.700 months (95%CI: 0.885-2.515). The median survival time of baseline CD4(+)T cell counts ≤ 50 /µl group was 1.670 months (95%CI: 0.759-2.581), and 51-199 /µl group was 4.400 months (95%CI: 2.735-6.065), and ≥ 200/µl group was 7.100 months (95%CI: 0.000-14.542). The survival time was significantly different among different baseline marital status groups, different WHO clinical stage groups, and different CD4(+)T cell counts groups. The mortality risk of Single (unmarried, divorced, separation, widowed) group was 0.641 times of the risk in married or cohabitation group. The mortality risk of WHO clinical stage III or IV was 1.856 times of the risk in stage I or II. The mortality risk of baseline CD4(+)T cell counts 51-199 /µl group was 0.582 times of the risk in ≤ 50 /µl group, and ≥ 200 /µl group was 0.551 times of the risk in ≤ 50 /µl group.

CONCLUSIONThe total median survival time was relatively short. Most AIDS deaths happened in the first 3 months or 3-6 months after they received Antiretroviral Therapy, and the mortality trend slowed down in the following months. Married or cohabitation, low-baseline CD4(+)T cell counts, or WHO clinical stage III or IV were found to be the risk factors associated with AIDS death cases receiving Antiretroviral Therapy.

Acquired Immunodeficiency Syndrome ; Antiretroviral Therapy, Highly Active ; CD4 Lymphocyte Count ; Cohort Studies ; Disease Progression ; HIV Infections ; Humans ; Marital Status ; Proportional Hazards Models ; Retrospective Studies ; Risk Factors ; Survival Rate