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HLA genotyping is a prerequisite for selection of suitable donors in the process of bone marrow transplantation. In the current study, the frequencies of HLA-A, -B, -C and -DRB1 alleles and A-B-C-DRB1 haplotypes were assessed in 855 healthy Iranian persons using a low-resolution sequence specific primer (SSP) kit. Frequencies were compared between 11 subpopulations including Armani, Balouch, Bandari, Turk, Turkaman, Arab, Fars, Kurd, Gilaki, Lor and Mazani. In total, 17 HLA-A alleles were detected, one of which (HLA-A*74) was present only among Lors. HLA-A*23 and -A*26 were the most frequent HLA-A alleles among Armanis. HLA-A*23 was also common among Turkamans. HLA-A*11 and -A*26 were most frequent among the Balouch subpopulation. The former allele was also frequent among Bandaris. HLA-A*02 was identified as the most common HLA-A allele among Turk, Arab and Fars subpopulations. HLA-A*30 were strongly enriched among Gilakis. A total of 31 HLA-B alleles were detected across the target population. While all alleles were present among Fars subgroup, Armanis and Turkamans had the lowest degree of diversity among the alleles examined. Moreover, HLA-B*35 and B*49 alleles were strongly enriched among Armanis and Turkamans, respectively. A total of 13 HLA-C alleles were identified across the population, all of which were present in the Fars subpopulation. HLA-C*03 and C*04 were the only HLA-C alleles identified among the Bandari subpopulation. HLA-DRB1*08 was not detected in any subpopulation other than Fars. HLA-DRB1*16 was significantly enriched among Bandaris. These data have practical significance in anthropological studies, disease association investigations and bone marrow transplantation.

Background: Natural killer cells (NKC) and Sorafenib (Sor) are two important agents for the treatment of hepatocellular carcinoma (HCC). Over the past decade, the interaction of Sor and NKC against HCC has been widely challenging. This study aimed to assess the efficacy of NKC & Sor for the treatment of HCC in vivo. Methods: Subcutaneous xenograft models of HCC were established in nude mice. For safety assessment of treatment, the kidney and liver functions were analyzed. Paraffin embedded tumor sections were histopathologically studied and immunohistochemistry (IHC) tests were done to evaluate the angiogenesis (CD34) and proliferation (Ki67) indexes. The terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay was performed to identify the tumor cells undergoing apoptosis. The serum levels of tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) were measured by enzyme-linked immunosorbent assay (ELISA) and expression levels of major inflammatory cytokines and cytoplasmic granules in xenograft HCC were quantified using real-time PCR. Results: NKC & Sor significantly inhibited necrosis and apoptosis in tumor cells and increased angiogenesis and proliferation of HCC compared to the monotherapy of NKC or Sor alone. The serum levels of TNF-α, IFN-γ as well as the expression levels of TNF-α, IFN-γ, interleukins (ILs)-1, 6, 10, granzyme-B and perforin in the xenograft HCC tissues of the treated mice with NKC & Sor were significantly lower than those of treated with NKC or Sor alone. Conclusion: Therapy with the specific dosage of NKC & Sor could not inhibit the HCC xenograft growth rate through a synergistic effect in a mouse model of HCC.

In this study, we reviewed various aspects of cytomegalovirus infection, including pathophysiology, diagnosis methods, and antiviral treatments. Background: Infections continue to be a major reason of complications like high non-relapse morbidity and mortality rate after allogenic hematopoietic stem cell transplantation. Cytomegalovirus is the most common infection in immunocompromised patients or those with graft-versus-host disease. The Latent-cytomegalovirus disease could increase the risk of reactivation in allogenic hematopoietic stem cell transplantation patients and lead to profound adverse effects on transplantation outcomes. Cytomegalovirus-specific CD4 + and CD8 + T cells reconstitution is crucial for protection against the virus reactivation. Different prophylactic, pre-emptive, and therapeutic anti-viral drugs are available to prevent cytomegalovirus infection/reactivation and treat resistant infections. Conclusion: Although there has been introduced various CMV antiviral treatment strategies like antiviral drugs, Vaccination, passive immunotherapies and adoptive transfer of CMV-specific T cells, further clinical trials are required to approve current therapies.