Human Leukocyte Antigens -DQA1 and -DQB1 Alleles in Patients With Common Warts.

Introduction The human papillomavirus induces the formation of lesions in different epithelia. Several studies describe an association of class II human leukocyte antigen with genital lesions, implying that they could also be related to the presence of common warts. The goal of this work was to determine the frequency of human leukocyte antigens (HLA)-DQA1 and HLA-DQB1 in Mexicans with common warts. Methods Thirty-two patients with a diagnosis of common warts, without any other systemic disease, and 100 healthy subjects from the same geographic area were recruited. The second exon of the HLA-DQA1 and HLA-DQB1 loci was typed by dot-blot and chemiluminescence. Results Alleles DQA1*03:01:01 (P = 0.021) and DQB1*03:02 (P = 0.036) were associated with the presence of skin warts. DQA1*04:01-DQB1*04:02 (P = 0.009) and DQA1*03:01:01-DQB1*03:02 (P = 0.044) were the most frequent haplotypes in patients. Conclusion In conclusion, the results of our study showed that the alleles DQA1 *03:01:01, DQB1*03:02, DQA1 *04:01, and DQB1*04:02 were associated with susceptibility to common warts, while DQA1*05:01 was significantly diminished in them. Consequently, the haplotypes DQA1*04:01-DQB1*04: 02 and DQA1*03:01:01-DQB1*03:02 were found to be associated with susceptibility, and DQA1*05:01-DQB1*03:01 increased significantly in controls. Therefore, the alleles of the DQA1 and DQB1 genes that are associated with susceptibility could be presenting human papillomavirus (HPV) peptides to T lymphocytes that activate a Th2-type response (anti-inflammatory cytokines), which allows the development of skin warts in this population.

p53 and p16 in oral epithelial dysplasia and oral squamous cell carcinoma: A study of 208 cases.

BACKGROUND: The use of p16 and p53 as biomarkers of malignant transformation of oral epithelial dysplasia (OED) and biological behavior of oral squamous cell carcinoma (OSCC) is controversial. AIM: To determine the immunoexpression of p16 and p53 in OED and OSCC and to establish their possible relation to histopathological grading of OED/OSCC. MATERIALS AND METHODS: Ninety-six OEDs (40 mild, 36 moderate, and 20 severe dysplasia); and 112 OSCCs (64 well-differentiated, 38 moderately differentiated, and 10 poorly differentiated) coming from archives of four centers of oral pathology were included. Histological slides from all cases were processed with immunohistochemical technique using anti-p53 and anti-p16 antibodies. The intensity of the immunoreactivity were classified using the ImageLab®MCM systemas follows: <60 mild, >60-<90 moderate, and >90 strong. Forstatistical purposesa χ2 test (P < 0.05) was performed. RESULTS: Severe dysplasia show highest relative frequency of p16-positive (35.5%), whereas p53 is associated with mild dysplasia (P = 0.04). Moderately differentiated OSCC had larger relative frequency of p16-positive and p53-positive cases (47.3% both circumstances) (P > 0.05). Statistical association of p16-positive and p53-positive cells to basal stratum of OED (P = 0.0008; P = 0.0000, respectively) and p16-positive cells and p53-positive cells to perivascular zone of OSCC (P = 0.001; P = 0.0000, respectively) was found. CONCLUSIONS: p16 and p53 could be not specific enough to identify patients suffering OED with high risk to malignancy; however, the evaluation of the presence of p16 and p53 in the tumoral invasive front of OSCC could contribute to establish the tumor progression.