Tehran University Medical Journal

Cancer/testis antigens (CTAs) are a kind of antigens that their expression mostly is restricted in testis and female’s genital organs. Tumor cells often express antigens whose expression is normally limited to germ cells. CTAs are composed of a vast gene family of closely related members and are commonly classified into two groups: the CT-X antigens that are encoded by the X chromosome and the non-X CTAs that are encoded by the autosomes. CTA are extensively and variably dispersed between tumors of diverse histotypes. CTA are broadly expressed in tumors, but not in normal tissue except for testis that is not available to the immune system, actually, the blood-testis barrier and the lack of HLA class I expression on the surface of germ cells avoid the immune system from the interaction with CTA proteins to be identified as non-self-structures. Consequently, CTA can be regarded as fundamentally tumor-specific targets. With extensive investigations on the function of this important biological molecules, their functions are somewhat revealed. Because of their high immunogenicity, tumor-limited, and biased expression, detection of these molecules provides unprecedented chances for further research and clinical development in the field of immunotherapy and cancer diagnosis. Also, growing evidence discloses that a number of CTAs stimulate epithelial mesenchymal transition (EMT) and generation of cancer stem-like cells, increasing metastasis, invasion and tumorigenesis. According to recent clinical attention, more features of CTA regulation are explored. CTA expression has been confirmed in a variety of human cancer tissues and some of them have been discovered to cause humoral and/or cellular immune responses in cancer patients, likewise, they displayed intertumor and intratumor heterogeneity in expression levels. CTAs are excellent targets for targeted tumor therapy, anticancer drug discovery, and diagnostic biomarkers, similarly, appreciated genes in the study of promoting tumorigenesis, immunotherapy, and malignant progression. This review summaries and classifies our current understanding of the complex and biased process of CTAs mRNA and protein expression in cancer, and provide the most current information on their function and regulation.
 

Behçet's disease (BD), also known as the Silk Road disease, is a multisystemic and rare inflammatory disorder primarily prevalent in populations along the Mediterranean Sea. Today, BD is defined as a crossroad between autoimmune and auto-inflammatory syndromes. Variety of syndromes including mucocutaneous manifestations such as oral and genital ulcers, papulopustular lesions and erythema nodosum as well as ocular, vascular, gastrointestinal and nervous system occur. The disease etiology has not yet been elaborated, though researchers have reported several reasons that can increase the likelihood of the disease occurrence including a genetic factor, human leukocyte antigen HLA-B51 (B51) antigen, infectious conditions such as herpes simplex virus (HSV), those involved in inflammatory and autoimmune conditions such as imbalance of various cytokines and immune cells levels as well as existence of various gene variants. Among the various immuno dysfunctions that are found in BD, patients have increased neutrophil motility and superoxide production, as well as elevated production of tumor necrosis factor (TNF)-α and decreased production of interleukin-10 (IL-10). Since vasculitis and tissue damage is usually seen with Behcet disease, unusual concentrations of chemokine and adhesion molecules can also help us understand the causes of disease. Among the functional deficiencies of the immune system, increased concentrations of neutrophils and monocytes are of importance leading to an increase in reactive oxygen species (ROS). Behcet's disease has common characteristics with some immune-mediated diseases such as systemic lupus erythematosus (SLE), psoriasis, ankylosing spondylitis, and inflammatory bowel disease (IBD), which suggests that they may share similar etiologies and genes. Genetic and epigenetic modulations have also been proposed as involved in the pathogenesis of BD. Modifications in DNA methylation have been found in BD patient monocytes and lymphocytes, leading to the adverse function of these cells. The positive replies to classical immunosuppressive agents like cyclosporine and azathioprine and participation of autoantigens at the beginning of the illness are the chief BD features that reflect the autoimmune nature of the disorder. This review article attempts to introduce the BD disease and its contributing factors with emphasis on the role of different cells and cytokines based on updated studies.