Anti-HLA-E Monoclonal antibody, clone 4E23IMB-F [PE]

Chronic hepatitis B virus (HBV) infection occurs in association to a deregulation of immune system. Human leukocyte antigen E (HLA-E) is an immune-tolerant nonclassical HLA class I molecule that could be involved in HBV progression. To measure soluble (s) HLA-E in patients with chronic HBV hepatitis (CHB). We tested the potential association of HLA-E*01:01/01:03 A > G gene polymorphism to CHB. Our cohort consisted of 93 Tunisian CHB patients (stratified in CHB with high HBV DNA levels and CHB with low HBV DNA levels) and 245 healthy donors. Plasma sHLA-E was determined using enzyme-linked immunosorbent assay (ELISA). Genotyping was performed using polymerase chain reaction sequence-specific primer. No association between HLA-E*01:01/01:03 A > G polymorphism and HBV DNA levels in CHB patients was found. G/G genotype is less frequent in CHB patients without significance. sHLA-E is significantly enhanced in CHB patients compared with healthy controls (P = 0.0017). Stratification according to HBV DNA levels showed that CHB patients with low HBV DNA levels have higher sHLA-E levels compared with CHB patients with high HBV DNA levels. CHB patients with G/G genotype have enhanced sHLA-E levels compared with other genotypes (P = 0.037). This significant difference is maintained only for CHB women concerning G/G genotypes (P = 0.042). Finally, we reported enhanced sHLA-E in CHB patients with advanced stages of fibrosis (P = 0.032). We demonstrate, for the first time, the association of sHLA-E to CHB. Owing to the positive correlation of HLA-E*01:01/01:03 A > G polymorphism and the association of sHLA-E to advanced fibrosis stages, HLA-E could be a powerful predictor for CHB progression. Further investigations will be required to substantiate HLA-E role as a putative clinical biomarker of CHB.

Objective: There is a strong relationship between the cancer stem cells (CSCs) and poor prognosis, metastasis and recurrence. In addition to this CSCs are resistant to chemotherapy and radiotherapy. Therefore, current treatment approaches may be ineffective to elimination of CSCs. The tumor cells have various adaptations for escaping from immune cells. The human leukocyte antigen (HLA)-G, which expressions restricted with fetal tissues and HLA-E are kind of tumor immune evasive adaptations. In this study, we aimed to investigate the relationship between the CSCs and immune evasive adaptations of breast tumors. Methods: We immunohistochemically evaluated that the expressions of cluster of differentiation (CD) 44, CD133, Homeobox protein Nanog, octamer-binding transcription factor (Oct) 3/4, HLA-G and HLA-E in the advanced stage breast cancer tissues (n= 10) and the non-malignant breast biopsies (n= 10). Results: We detected that the significantly increased expressions of especially Nanog (p< 0.001) and also CD44 (p< 0.001), CD133 (p< 0.001) and Oct3/4 (p< 0.001) in the advanced stage breast tumor group compared with non-malignant breast biopsies group, but the HLA-G (p< 0.001) and HLA-E (p< 0.001) decreased. Conclusion: These findings suggested that, malignant breast tumors may have CSC-like cells, and these cells may play role for occurring malignant behavior. To proliferation and tumor formation, the immune evasion is essential for both of malignant and benign tumors. Higher expressions of HLA-G and HLA-E may be an indication that the non-malign tumors more immune evasive than the malign tumors. However, further prospective studies are needed to confirm our findings.